目录号 | 产品详情 | 靶点 | |
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T19777 | Apoptosis Others Guanylate cyclase | ||
ODQ 是一种选择性可溶性的鸟苷酰环化酶抑制剂,可增强顺铂促人间皮瘤细胞凋亡的作用。 | |||
T8405 | PDE | ||
Vardenafil hydrochloride 是口服具有活性的、高效的、选择性的磷酸二酯酶 5抑制剂。它对 PDE1 (180 nM),PDE6 (11 nM),PDE2,PDE3,PDE4 (>1000 nM) 具有选择性。它能够非竞争性地抑制环磷酸鸟苷水解,提高 cGMP 水平。它可用于勃起功能障碍的研究。 | |||
T8348 | Adrenergic Receptor | ||
Phentolamine 是一种 alpha-1 和 alpha-2 选择性肾上腺素能受体拮抗剂。 | |||
T0866 | Potassium Channel MRP Sodium Channel | ||
Propafenone (Propafenonum) 是钠通道阻滞剂,它对 β 受体具有高亲和力 (IC50=32 nM)。它能够阻断瞬时外向钾电流 (Ito) (IC50: 4.9 nM) 和持续延迟整流器K+电流 (Isus) (IC50: 8.6 nM) ,具有抗心律失常的作用。它能够诱导线粒体功能障碍及诱导细胞凋亡,从而抑制食管癌增殖。 | |||
T1635 | AChE Parasite | ||
Fenchlorphos (Dermafos) 是一种有机磷酸盐杀虫剂,是乙酰胆碱酯酶的抑制剂,能够引起线粒体功能障碍。 | |||
T11685 | Apoptosis Others | ||
Isolongifolene ((-)-Isolongifolene) 是一种从调料九里香中分离的三环倍半萜烯,具有抗氧化,抗炎,抗癌和神经保护的特性。它通过调节 PI3K/AKT/GSK-3β 信号通路来减轻鱼藤酮诱导的氧化应激,线粒体功能障碍和细胞凋亡。 | |||
T0096 | PDE | ||
Vardenafil (Vivanza) 是选择性、高效的、具有口服活性的磷酸二酯酶5抑制剂,IC50=0.7 nM。它能够非竞争性地抑制环磷酸鸟苷水解,从而提高 cGMP 水平。它对 PDE1 (180 nM),PDE6 (11 nM),PDE2,PDE3,PDE4 (>1000 nM) 具有选择性。它可用于研究勃起功能障碍。 | |||
TN4417 | Others | ||
Larixyl acetate 是一种生物活性化学物质。 | |||
TQ0091 | Opioid Receptor | ||
LY2795050 是一种新型特异性 κ-阿片受体拮抗剂,IC50为0.72 nM。 | |||
T22671 | 5-HT Receptor | ||
CJ 033466 是 5-HT4 受体 (EC50 = 9 nM) 的特异性部分激动剂,具有促胃动力作用。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02881 | RAGE Protein, Human, Recombinant | Human | HEK293 | ||
Receptor for Advanced Glycosylation End Products (RAGE, or AGER) is a member of the immunoglobulin super-family transmembrane proteins, as a signal transduction receptor which binds advanced glycation endproducts, certain members of the S100/calgranulin family of proteins, high mobility group box 1 (HMGB1), advanced oxidation protein products, and amyloid (beta-sheet fibrils). Initial studies investigating the role of RAGE in renal dysfunction focused on diabetes, neurodegenerative disorders, and inflammatory responses. However, RAGE also has roles in the pathogenesis of renal disorders that are not associated with diabetes, such as obesity-related glomerulopathy, doxorubicin-induced nephropathy, hypertensive nephropathy, lupus nephritis, renal amyloidosis, and ischemic renal injuries. RAGE represents an important factor in innate immunity against pathogens, but it also interacts with endogenous ligands, resulting in chronic inflammation. RAGE signaling has been implicated in multiple human illnesses, including atherosclerosis, arthritis, Alzheimer's disease, atherosclerosis and aging associated diseases.
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TMPY-02927 | RAGE Protein, Human, Recombinant (His) | Human | HEK293 | ||
Receptor for Advanced Glycosylation End Products (RAGE, or AGER) is a member of the immunoglobulin super-family transmembrane proteins, as a signal transduction receptor which binds advanced glycation endproducts, certain members of the S100/calgranulin family of proteins, high mobility group box 1 (HMGB1), advanced oxidation protein products, and amyloid (beta-sheet fibrils). Initial studies investigating the role of RAGE in renal dysfunction focused on diabetes, neurodegenerative disorders, and inflammatory responses. However, RAGE also has roles in the pathogenesis of renal disorders that are not associated with diabetes, such as obesity-related glomerulopathy, doxorubicin-induced nephropathy, hypertensive nephropathy, lupus nephritis, renal amyloidosis, and ischemic renal injuries. RAGE represents an important factor in innate immunity against pathogens, but it also interacts with endogenous ligands, resulting in chronic inflammation. RAGE signaling has been implicated in multiple human illnesses, including atherosclerosis, arthritis, Alzheimer's disease, atherosclerosis and aging associated diseases.
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TMPY-03762 | E-Cadherin/Cadherin-1 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Cadherins are calcium-dependent cell adhesion proteins which preferentially interact with themselves in a homophilic manner in connecting cells, and thus may contribute to the sorting of heterogeneous cell type. E-cadherin (E-Cad), also known as CDH1 and CD324, is a calcium-dependent cell adhesion molecule the intact function of which is crucial for the establishment and maintenance of epithelial tissue polarity and structural integrity. Mutations in CDH1 occur in diffuse type gastric cancer, lobular breast cancer, and endometrial cancer. In human cancers, partial or complete loss of E-cadherin expression correlates with malignancy. During apoptosis or with calcium influx, E-Cad is cleaved by the metalloproteinase to produce fragments of about 38 kDa (E-CAD/CTF1), 33 kDa (E-CAD/CTF2) and 29 kDa (E-CAD/CTF3), respectively. E-Cad has been identified as a potent invasive suppressor, as downregulation of E-cadherin expression is involved in dysfunction of the cell-cell adhesion system, and often correlates with strong invasive potential and poor prognosis of human carcinomas.
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TMPY-01650 | CD131 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Colony stimulating factor 2 receptor, beta, low-affinity (CSF2RB) also known as CD131 antigen (CD131), cytokine receptor common subunit beta, GM-CSF/IL-3/IL-5 receptor common beta-chain, interleukin 3 receptor/granulocyte-macrophage colony stimulating factor 3 receptor, beta (IL3RB), is the common beta chain of the high affinity receptor for IL-3, IL-5 and CSF. Defects in this protein have been reported to be associated with protein alveolar proteinosis (PAP). CD131 belongs to the type I cytokine receptor family. The cluster of differentiation (cluster of designation) (often abbreviated as CD) is a protocol used for the identification and investigation of cell surface molecules present on white blood cells initially but found in almost any kind of cell of the body, providing targets for immunophenotyping of cells. Defects in CD131/CSF2RB are the cause of pulmonary surfactant metabolism dysfunction type 5 (SMDP5). SMDP5 is a rare lung disorder due to impaired surfactant homeostasis. It is characterized by alveolar filling with floccular material that stains positive using the periodic acid-Schiff method and is derived from surfactant phospholipids and protein components. Excessive lipoproteins accumulation in the alveoli results in severe respiratory distress.
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TMPY-01028 | Ficolin 1/FCN1 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Ficolins are humoral molecules of the innate immune systems which recognize carbohydrate molecules on pathogens, apoptotic and necrotic cells. The Ficolin family of proteins are characterized by the presence of a leader peptide, a short N-terminal segment, followed by a collagen-like region, and a C-terminal fibrinogen-like domain. Ficolins are humoral molecules of the innate immune systems which recognize carbohydrate molecules on pathogens, apoptotic and necrotic cells. Three Ficolins have been identified in humans: L-Ficolin, H-Ficolin and M-Ficolin (also referred to as Ficolin-2, -3 and -1, respectively). They are soluble oligomeric defence proteins with lectin-like activity and they are structurally similar to the human collectins, mannan-binding lectin (MBL) and surfactant protein A and D. Dysfunction or abnormal expressions of Ficolins may involved in the pathogenesis of human diseases including infectious and inflammatory diseases, autoimmune disease and clinical syndrome of preeclampsia. They are soluble oligomeric defence proteins with lectin-like activity and they are structurally similar to the human collectins, mannan-binding lectin (MBL) and surfactant protein A and D. Upon recognition of the infectious agent, the Ficolins act through two distinct routes: initiate the lectin pathway of complement activation through attached serine proteases (MASPs), and a primitive opsonophagocytosis thus limiting the infection and concurrently orchestrating the subsequent adaptive clonal immune response. Ficolin-1 (FCN1) is predominantly expressed in the peripheral blood leukocytes.
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TMPY-01725 | Leptin Receptor Protein, Human, Recombinant (His) | Human | HEK293 | ||
Leptin Receptor or CD295 belongs to the gp130 family of cytokine receptors that are known to stimulate gene transcription via activation of cytosolic STAT proteins. This protein is a receptor for leptin (an adipocyte-specific hormone that regulates body weight) and is involved in the regulation of fat metabolism, as well as in a novel hematopoietic pathway that is required for normal lymphopoiesis. Leptin Receptor/CD295 is transmembrane catalytic receptors found on NPY/AgRP and alpha-MSH/CART neurons in hypothalamic nuclei. Leptin receptors (Ob-Rs) are coded for by one human gene that produces six different isoforms; Ob-Ra - Ob-Rf. Ob-Rs exist as constitutive dimers at physiological expression levels. Only the Ob-Rb isoform can transduce intracellular signals and does so through activation of the JAK2/STAT3, PI 3-K, and MAPK signaling cascades. Activation of Ob-Rs mediates transcriptional regulation of the hypothalamic melanocortin pathway and downregulates endocannabinoid expression. Leptin acts via leptin receptors. Leptin resistance has been proposed as a pathophysiological mechanism of obesity. In obese individuals, Ob-Ra (which is involved in the active transport of leptin across the blood-brain barrier) expression is downregulated and the individual may be unresponsive to leptin signals. Ob-R antagonists are of great interest in the development of pharmacological treatments for obesity. Mutations in the Leptin Receptor/CD295 have been associated with obesity and pituitary dysfunction.
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TMPY-00635 | IL-7R alpha/CD127 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
Interleukin 7 Receptor alpha (IL-7RA), also known as CD127, is a 75 kDa hematopoietic receptor superfamily member that plays an important role in lymphocyte differentiation, proliferation, and survival. IL-7 receptor alpha (CD127) signaling is essential for T-cell development and regulation of naive and memory T-cell homeostasis. IL-7RA is critically required for the proper development and function of lymphoid cells. Therefore, the IL-7RA is critically required for the proper development and function of lymphoid cells. Studies from both pathogenic and controlled HIV infection indicate that the containment of immune activation and preservation of CD127 expression are critical to the stability of CD4(+) T cells in infection. A better understanding of the factors regulating CD127 expression in HIV disease, particularly on T(CM) cells, might unveil new approaches exploiting the IL-7/IL-7R receptor pathway to restore T cell homeostasis and promote immune reconstitution in HIV infection. Factors relevant to HIV infection that could potentially decrease CD127 expression on human CD8(+) T cells. CD127 down-regulation may be an important contributor to HIV-associated T-cell dysfunction. In addition to IL-7, IL-7RA also associates with TSLPR to form the functional receptor for thymic stromal lymphopoietin (TSLP) which indirectly regulates T cell development by modulating dendritic cell activation. Mutations in the human IL-7RA gene cause a type of severe combined immunodeficiency in which the major deficiencies are in T cell development, whereas B and NK cells are relatively normal in number. Variation in the IL7RA gene was recently found associated with multiple sclerosis (MS). The polymorphisms in the IL7RA gene is involved in MS pathogenesis and suggest that IL7RA variation may primarily affect chronic disease courses. Soluble CD127 (sCD127) appears to play an important role in the immunopathogenesis of several chronic infections, multiple sclerosis, and various cancers.
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TMPY-01209 | IL-7R alpha/CD127 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Interleukin 7 Receptor alpha (IL-7RA), also known as CD127, is a 75 kDa hematopoietic receptor superfamily member that plays an important role in lymphocyte differentiation, proliferation, and survival. IL-7 receptor alpha (CD127) signaling is essential for T-cell development and regulation of naive and memory T-cell homeostasis. IL-7RA is critically required for the proper development and function of lymphoid cells. Therefore, the IL-7RA is critically required for the proper development and function of lymphoid cells. Studies from both pathogenic and controlled HIV infection indicate that the containment of immune activation and preservation of CD127 expression are critical to the stability of CD4(+) T cells in infection. A better understanding of the factors regulating CD127 expression in HIV disease, particularly on T(CM) cells, might unveil new approaches exploiting the IL-7/IL-7R receptor pathway to restore T cell homeostasis and promote immune reconstitution in HIV infection. Factors relevant to HIV infection that could potentially decrease CD127 expression on human CD8(+) T cells. CD127 down-regulation may be an important contributor to HIV-associated T-cell dysfunction. In addition to IL-7, IL-7RA also associates with TSLPR to form the functional receptor for thymic stromal lymphopoietin (TSLP) which indirectly regulates T cell development by modulating dendritic cell activation. Mutations in the human IL-7RA gene cause a type of severe combined immunodeficiency in which the major deficiencies are in T cell development, whereas B and NK cells are relatively normal in number. Variation in the IL7RA gene was recently found associated with multiple sclerosis (MS). The polymorphisms in the IL7RA gene is involved in MS pathogenesis and suggest that IL7RA variation may primarily affect chronic disease courses. Soluble CD127 (sCD127) appears to play an important role in the immunopathogenesis of several chronic infections, multiple sclerosis, and various cancers.
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TMPK-00751 | FSTL3 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Follistatin-like 3 (FSTL3) is a novel cytokine that regulates insulin sensitivity and counteracts activin/myostatin signalling. In the present study, regulation of FSTL3 in renal dysfunction was investigated in both human chronic kidney disease (CKD) and acute kidney dysfunction (AKD). Furthermore, mFSTL3 expression was analysed in insulin-sensitive tissues in a mouse model of CKD.
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TMPY-03227 | CISD1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Mitochondrial dysfunction is thought to play a significant role in neurodegeneration observed in Parkinson's disease (PD), the loss of mitoNEET (CISD1), an iron-sulfur containing protein that regulates mitochondrial bioenergetics, results in mitochondrial dysfunction and loss of striatal dopamine and tyrosine hydroxylase. CDGSH iron sulfur domain 1 (CISD1, also termed mitoNEET), an iron-containing outer mitochondrial membrane protein, negatively regulates ferroptotic cancer cell death. At the cellular level, CISD1 gene expression increased during human adipocyte differentiation in correlation with adipogenic genes.Thus it is a possible role of CISD1 in obesity-associated dysfunctional adipogenesis in human VAT.
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TMPJ-01083 | Serpin E2 Protein, Mouse, Recombinant (His) | Mouse | Human Cells | ||
Serpin E2 is a member of the Serpin superfamily. It is differentially expressed during neuronal differentiation and is able to transform human embryonic kidney cells into neuronlike cells. Its over-expression in mice leads to progressive neuronal and motor dysfunction in these animals. It is also over-expressed in the majority of pancreatic carcinoma as well as gastric and colorectal cancer samples whereas it is weakly expressed in all normal pancreas and chronic pancreatitis tissue samples. Serpin E2 is a potent inhibitor of thrombin, trypsin, urokinase, plasmin and plasminogen activators. It plays an important role in controlling male fertility because its knockout male mice show a marked impairment in fertility from the onset of sexual maturity and its abnormal expression is found in the semen of men with seminal dysfunction.
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TMPY-00518 | SBDS Protein, Human, Recombinant (His) | Human | E. coli | ||
The mutation of Shwachman-Bodian-Diamond syndrome (SBDS) gene has been proposed to be a major causative reason for SDS. Shwachman-Diamond syndrome (SDS) is a rare pediatric disease characterized by various systemic disorders, including hematopoietic dysfunction. SBDS deficiency leads to telomere shortening, that SBDS is a telomere-protecting protein that participates in regulating telomerase recruitment.
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TMPH-03728 | Zaire ebolavirus (strain Kikwit-95) VP40 Protein (His & Myc) | ZEBOV | Baculovirus | ||
Plays an essential role virus particle assembly and budding. Acts by interacting with viral ribonucleocapsid and host members of the ESCRT (endosomal sorting complex required for transport) system such as host VPS4, PDCD6IP/ALIX, NEDD4 or TGS101. The interaction with host E3 ubiquitin ligase SMURF2 also facilitates virus budding. May play a role in immune cell dysfunction by being packaged into exosomes that can decrease the viability of recipient cells (via RNAi suppression and exosome-bystander apoptosis).
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TMPY-04773 | TPK1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Thiamine pyrophosphokinase (TPK) produces thiamine pyrophosphate, a cofactor for a number of enzymes, including pyruvate dehydrogenase and 2-ketoglutarate dehydrogenase. Episodic encephalopathy type thiamine metabolism dysfunction (OMIM 614458) due to TPK1 mutations is a recently described rare disorder. The genomic variations in the fetal and maternal TPK1 gene could contribute to the variability of birth weight in normal humans.
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TMPY-00452 | SBDS Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
The mutation of Shwachman-Bodian-Diamond syndrome (SBDS) gene has been proposed to be a major causative reason for SDS. Shwachman-Diamond syndrome (SDS) is a rare pediatric disease characterized by various systemic disorders, including hematopoietic dysfunction. SBDS deficiency leads to telomere shortening, that SBDS is a telomere-protecting protein that participates in regulating telomerase recruitment.
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TMPJ-01002 | SGSH Protein, Human, Recombinant (His) | Human | Human Cells | ||
N-Sulphoglucosamine Sulphohydrolase (SGSH) is an important member of the sulfatase family which is involved in the degradation of heparin sulfate. SGSH binds one calcium ion per subunit as a cofactor. SGSH catalyzes N-sulfo-D-glucosamine and H2O to D-glucosamine and sulfate. SGSH deficiency is result in mucopolysaccharidosis type 3A (MPS3A), a recessive lysosomal storage disease characterized by neurological dysfunction but relatively mild somatic manifestations.
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TMPY-03353 | CEL Protein, Mouse, Recombinant (His) | Mouse | Baculovirus-Insect Cells | ||
CEL-maturity onset diabetes of the young (MODY), diabetes with pancreatic lipomatosis and exocrine dysfunction, is due to dominant frameshift mutations in the acinar cell carboxyl ester lipase gene (CEL). Bile-salt activated carboxylic ester lipase (CEL) is a major triglyceride, cholesterol ester and vitamin ester hydrolytic enzyme contained within pancreatic and lactating mammary gland secretions. Carboxyl ester lipase is a digestive pancreatic enzyme encoded by the CEL gene. Mutations in CEL cause maturity-onset diabetes of the young as well as pancreatic exocrine dysfunction. The enzyme carboxyl ester lipase (CEL), also known as bile salt-dependent or -stimulated lipase (BSDL, BSSL), hydrolyzes dietary fat, cholesteryl esters and fat-soluble vitamins in the duodenum. CEL is mainly expressed in pancreatic acinar cells and lactating mammary glands. The human CEL gene resides on chromosome 9q34.3 and contains a variable number of tandem repeats (VNTR) region that encodes a mucin-like protein tail.
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TMPY-01929 | ECE1 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Endothelin-converting enzyme 1, also known as ECE-1, is a single-pass type II membrane protein which belongs to thepeptidase M13 family. ECE-1 converts big endothelin-1 to endothelin-1. ECE-1 is a membrane metalloprotease that generates endothelin from its direct precursor big endothelin. Four isoforms of ECE-1 are produced from a single gene through the use of alternate promoters. These isoforms share the same extracellular catalytic domain and contain unique cytosolic tails, which results in their specific subcellular targeting.All isoforms of ECE-1 are expressed in umbilical vein endothelial cells, polynuclear neutrophils, fibroblasts, atrium cardiomyocytes and ventricles. Isoforms A, B and C of ECE-1 are also expressed in placenta, lung, heart, adrenal gland and phaeochromocytoma; isoforms A and C of ECE-1 in liver, testis and small intestine; isoform B, C and D of ECE-1 in endothelial cells and umbilical vein smooth muscle cells; isoforms C and D in saphenous vein cells, and isoform C in kidney. Defects in ECE1 are a cause of Hirschsprung disease, cardiac defects and autonomic dysfunction. It is a form of Hirschsprung disease with skip-lesions defects, craniofacial abnormalities and other dysmorphic features, and autonomic dysfunction.
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TMPJ-00834 | ACADM Protein, Human, Recombinant (His) | Human | E. coli | ||
Medium-Chain Specific Acyl-CoA Dehydrogenase (ACADM) is a mitochondrial fatty acid beta-oxidation that belongs to the acyl-CoA dehydrogenase family. ACADM is a homotetramer enzyme that catalyzes the initial step of the mitochondrial fatty acid beta-oxidation pathway. ACADM is specific for acyl chain lengths of 4 to 16. It is essential for converting these particular fatty acids to energy, especially during fasting periods. Defects in ACADM cause medium-chain acyl-CoA dehydrogenase deficiency, a disease characterized by hepatic dysfunction, fasting hypoglycemia, and encephalopathy, which can result in infantile death.
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TMPH-03727 | Zaire ebolavirus (strain Kikwit-95) VP40 Protein (His) | ZEBOV | E. coli | ||
Plays an essential role virus particle assembly and budding. Acts by interacting with viral ribonucleocapsid and host members of the ESCRT (endosomal sorting complex required for transport) system such as host VPS4, PDCD6IP/ALIX, NEDD4 or TGS101. The interaction with host E3 ubiquitin ligase SMURF2 also facilitates virus budding. May play a role in immune cell dysfunction by being packaged into exosomes that can decrease the viability of recipient cells (via RNAi suppression and exosome-bystander apoptosis).
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TMPK-01069 | TMEM106B Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
TMEM106B is a well-recognised risk factor for FTD caused by GRN mutation. Elegant experiments have suggested that increased risk for FTD is due to elevated levels of TMEM106B (Nicholson et al, 2013; Gallagher et al, 2017). Therefore, recent work has explored the therapeutic potential of reducing TMEM106B levels, with initial results looking encouraging, as crossing a Grn-deficient mouse to a Tmem106b knockout showed a rescue in FTD-related behavioural defects and specific aspects of lysosome dysfunction (Klein et al, 2017).
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TMPY-03175 | Claudin-11 Protein, Human, Recombinant (mFc) | Human | HEK293 | ||
Claudin-11, also known as CLDN11, belongs to the group of claudins. Claudins are integral membrane proteins and components of tight junction strands. Tight junction strands function as a physical barrier to prevent solutes and water from passing freely through the paracellular space between epithelial or endothelial cell sheets, and also play critical roles in maintaining cell polarity and signal transductions.Claudin-11 is a tight junction associated protein and is a major component of central nervous system (CNS) myelin that is necessary for normal CNS function. Human blood-testis barrier disruption is related to a dysfunction of CLDN11 gene. It plays an important role in regulating proliferation and migration of oligodendrocytes.
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TMPY-01350 | TIM-1/KIM-1/HAVCR1 Protein, Canine, Recombinant (His) | Canine | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-01455 | TIM-1/KIM-1/HAVCR1 Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-04620 | Neurofascin Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
NFASC (Neurofascin, also known as NRCAML, NEDCPMD, and NF) is a Protein Coding gene. 13 alternatively spliced human isoforms have been reported. NFASC belongs to the immunoglobulin superfamily, L1/neurofascin/NgCAM family. It contains 5 fibronectin type-III domains and 6 Ig-like C2-type (immunoglobulin-like) domains. The protein functions in neurite outgrowth, neurite fasciculation, and organization of the axon initial segment (AIS) and nodes of Ranvier on axons during early development. NFASC links the AIS extracellular matrix to the intracellular cytoskeleton. It is broadly expressed in the brain, kidney, and other tissues. Diseases associated with NFASC include Neurodevelopmental Disorder With Central And Peripheral Motor Dysfunction and Demyelinating Polyneuropathy.
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TMPY-01951 | TIM-1/KIM-1/HAVCR1 Protein, Rhesus, Recombinant | Rhesus | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-01768 | TIM-1/KIM-1/HAVCR1 Protein, Human, Recombinant (His) | Human | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-01671 | TIM-1/KIM-1/HAVCR1 Protein, Rhesus, Recombinant (His) | Rhesus | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-06810 | SFTPB Protein, Human, Recombinant (His) | Human | CHO | ||
Pulmonary surfactant-associated protein B, also known as SFTPB and SP-B, contains one saposin A-type domain and three saposin B-type domains. SP-B is produced primarily by alveolar type II cells (AEC2) but also by nonciliated respiratory epithelial cells lining distal portions of the respiratory tract. Its secretion promotes alveolar homeostasis, stabilizing lipid layers and lowering surface tension at the air-liquid interface in the peripheral air spaces. Alveolar SP-B influences surfactant formation, effector cell functions, and innate host defense. Deficiency is associated with respiratory distress syndrome (RDS), pulmonary surfactant metabolism dysfunction 1 (SMDP1), and other human lung diseases. Gene addition and editing therapies show promise by complementing SP-B expression in AEC2s, restoring the phenotypic defect in vitro and in vivo.
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TMPY-03797 | Neurofascin Protein, Human, Recombinant (His) | Human | HEK293 | ||
NFASC (Neurofascin, also known as NRCAML, NEDCPMD, and NF) is a Protein Coding gene. 13 alternatively spliced human isoforms have been reported. NFASC belongs to the immunoglobulin superfamily, L1/neurofascin/NgCAM family. It contains 5 fibronectin type-III domains and 6 Ig-like C2-type (immunoglobulin-like) domains. The protein functions in neurite outgrowth, neurite fasciculation, and organization of the axon initial segment (AIS) and nodes of Ranvier on axons during early development. NFASC links the AIS extracellular matrix to the intracellular cytoskeleton. It is broadly expressed in the brain, kidney, and other tissues. Diseases associated with NFASC include Neurodevelopmental Disorder With Central And Peripheral Motor Dysfunction and Demyelinating Polyneuropathy.
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TMPY-00668 | APP/Protease nexin-II Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Amyloid precursor protein (APP) is a type I transmembrane protein expressed in many tissues and concentrated in the synapses of neurons, and is suggested as a regulator of synapse formation and neural plasticity. APP can be processed by two different proteolytic pathways. In one pathway, APP is cleaved by β- and γ-secretase to produce the amyloid-β-protein (Aβ, Abeta, beta-amyloid) which is the principal component of the amyloid plaques, the major pathological hallmark of Alzheimer’s disease (AD), while in the other pathway, α-secretase is involved in the cleavage of APP whose product exerts antiamyloidogenic effect and prevention of the Aβ peptide formation. The aberrant accumulation of aggregated beta-amyloid peptides (Abeta) as plaques is a hallmark of AD neuropathology and reduction of Abeta has become a leading direction of emerging experimental therapies for the disease. Besides this pathological function of Abeta, recently published data reveal that Abeta also has an essential physiological role in lipid homeostasis. Cholesterol increases Abeta production, and conversely A beta production causes a decrease in cholesterol synthesis. Abeta may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level, but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. Abeta-induced dysfunction of inhibitory interneurons likely increases synchrony among excitatory principal cells and contributes to the destabilization of neuronal networks. There is evidence that beta-amyloid can impair blood vessel function. Vascular beta-amyloid deposition, also known as cerebral amyloid angiopathy, is associated with vascular dysfunction in animal and human studies. Alzheimer disease is associated with morphological changes in capillary networks, and soluble beta-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli.
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TMPY-02394 | IMPA1 Protein, Human, Recombinant (His) | Human | E. coli | ||
IMPA1 (Inositol Monophosphatase 1) is a Protein Coding gene. This gene encodes an enzyme that dephosphorylates Myo-inositol monophosphate to generate free Myo-inositol, a precursor of phosphatidylinositol, and is, therefore, an important modulator of intracellular signal transduction via the production of the second messenger's myoinositol 1,4,5-trisphosphate and diacylglycerol. Despite its many physiological functions, no clinical phenotype has been assigned to this gene dysfunction to date. Additionally, IMPA1 is the main target of lithium, a drug that is at the forefront of treatment for bipolar disorder. IMPA1 is widely expressed in the testis, thyroid, and other tissues. Diseases associated with IMPA1 include Mental Retardation, Autosomal Recessive 59, and Bipolar Disorder.
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TMPY-05268 | Neurofascin Protein, Human, Recombinant (hFc), Biotinylated | Human | HEK293 | ||
NFASC (Neurofascin, also known as NRCAML, NEDCPMD, and NF) is a Protein Coding gene. 13 alternatively spliced human isoforms have been reported. NFASC belongs to the immunoglobulin superfamily, L1/neurofascin/NgCAM family. It contains 5 fibronectin type-III domains and 6 Ig-like C2-type (immunoglobulin-like) domains. The protein functions in neurite outgrowth, neurite fasciculation, and organization of the axon initial segment (AIS) and nodes of Ranvier on axons during early development. NFASC links the AIS extracellular matrix to the intracellular cytoskeleton. It is broadly expressed in the brain, kidney, and other tissues. Diseases associated with NFASC include Neurodevelopmental Disorder With Central And Peripheral Motor Dysfunction and Demyelinating Polyneuropathy.
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TMPY-01317 | TIM-1/KIM-1/HAVCR1 Protein, Rat, Recombinant (His & hFc) | Rat | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPH-02322 | SLC30A10 Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Plays a pivotal role in manganese transport. Manganese is an essential cation for the function of several enzymes, including some crucially important for the metabolism of neurotransmitters and other neuronal metabolic pathways. However, elevated levels of manganese are cytotoxic and induce oxidative stress, mitochondrial dysfunction and apoptosis. Acts as manganese efflux transporter and confers protection against manganese-induced cell death. Also acts as zinc transporter involved in zinc homeostasis. Seems to mediate zinc transport into early endosomes and recycling endosomes to prevent zinc toxicity; the function may be regulated by heterodimerization with other zinc transporters of the SLC30A subfamily. The SLC30A3:SLC30A10 heterodimer is involved in zinc transport-dependent regulation of the EGFR/ERK transduction pathway in endosomes. May be involved in regulation of zinc-dependent senescence of vascular smooth muscle cells.
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TMPY-03349 | CD302 Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
CD302/CLEC13A (C-type lectin domain family 13 member A), also known as C-type lectin receptor DCL-1, is a type I transmembrane C-type lectin DCL-1/CD302. DCL-1 protein was highly conserved among the human, mouse, and rat orthologs. DCL-1 ectodomain contains only one CRD, whereas other type I transmembrane C-type lectins contain more than one domain (e.g. selectins and MMR). DCL-1 CP contains several putative motifs, including a Tyr-based internalization, a cluster of acidic amino acids, and Ser and Tyr phosphorylation motifs, suggesting that DCL-1 CP mediates not only endocytosis and late endosome targeting but also signaling. DCL-1 may be another cell/matrix adhesion receptor integrated in cell adhesion complexes and that DCL-1 dysfunction may affect APC adhesion and migration, causing suppression of APC function.
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TMPY-03884 | Beta-amyloid 39/Beta-APP39 Protein, Human, Recombinant (aa 672-710, His & GST) | Human | E. coli | ||
Amyloid precursor protein (APP) is a type I transmembrane protein expressed in many tissues and concentrated in the synapses of neurons, and is suggested as a regulator of synapse formation and neural plasticity. APP can be processed by two different proteolytic pathways. In one pathway, APP is cleaved by β- and γ-secretase to produce the amyloid-β-protein (Aβ, Abeta, beta-amyloid) which is the principal component of the amyloid plaques, the major pathological hallmark of Alzheimer’s disease (AD), while in the other pathway, α-secretase is involved in the cleavage of APP whose product exerts antiamyloidogenic effect and prevention of the Aβ peptide formation. The aberrant accumulation of aggregated beta-amyloid peptides (Abeta) as plaques is a hallmark of AD neuropathology and reduction of Abeta has become a leading direction of emerging experimental therapies for the disease. Besides this pathological function of Abeta, recently published data reveal that Abeta also has an essential physiological role in lipid homeostasis. Cholesterol increases Abeta production, and conversely A beta production causes a decrease in cholesterol synthesis. Abeta may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level, but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. Abeta-induced dysfunction of inhibitory interneurons likely increases synchrony among excitatory principal cells and contributes to the destabilization of neuronal networks. There is evidence that beta-amyloid can impair blood vessel function. Vascular beta-amyloid deposition, also known as cerebral amyloid angiopathy, is associated with vascular dysfunction in animal and human studies. Alzheimer disease is associated with morphological changes in capillary networks, and soluble beta-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli.
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TMPY-01244 | TIM-1/KIM-1/HAVCR1 Protein, Mouse, Recombinant (His & hFc) | Mouse | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-04280 | TIM-1/KIM-1/HAVCR1 Protein, Canine, Recombinant (mFc) | Canine | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-01161 | TIM-1/KIM-1/HAVCR1 Protein, Human, Recombinant (His & hFc) | Human | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPY-01173 | TIM-1/KIM-1/HAVCR1 Protein, Human, Recombinant (aa 1-135, His) | Human | HEK293 | ||
HAV cellular receptor 1 (HAVCR1), also known as Kidney injury molecule 1 (KIM-1) and T cell immunoglobulin mucin 1 (TIM-1), is a type of integral membrane glycoprotein. KIM-1 protein is widely expressed with the highest levels in the kidney and testis. It has been shown to play a major role as a human susceptibility gene for asthma, allergy, and autoimmunity. IgA1lambda is a specific ligand of KIM-1 protein and that their association has a synergistic effect in virus-receptor interactions. KIM-1 involves in the pathogenesis of acute kidney injury. It had been confirmed that KIM-1 is a human urinary renal dysfunction biomarker. Moreover, KIM-1 protein is a novel regulatory molecule of flow-induced calcium signaling.
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TMPJ-00796 | Serpin E2 Protein, Human, Recombinant (His) | Human | Human Cells | ||
Serpin E2 is a secreted protein that belongs to the serpin family. Serpin E2 is a serine protease inhibitor with activity toward thrombin, trypsin, and urokinase. Serpin E2 expression is weak or absent in all normal pancreas and chronic pancreatitis tissue. In contrast, it was strongly over-expressed in the majority of pancreatic carcinoma as well as gastric and colorectal cancer samples. Serpin E2 promotes neurite extension by inhibiting thrombin. It also can bind heparin. It has been shown that Serpin E2 is a novel target of ERK signaling involved in human colorectal tumorigenesis. It plays an important role in controlling male fertility because its knockout male mice show a marked impairment in fertility from the onset of sexual maturity and its abnormal expression is found in the semen of men with seminal dysfunction.
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TMPY-02406 | CD302 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
CD302/CLEC13A (C-type lectin domain family 13 member A), also known as C-type lectin receptor DCL-1, is a type I transmembrane C-type lectin DCL-1/CD302. DCL-1 protein was highly conserved among the human, mouse, and rat orthologs. DCL-1 ectodomain contains only one CRD, whereas other type I transmembrane C-type lectins contain more than one domain (e.g. selectins and MMR). DCL-1 CP contains several putative motifs, including a Tyr-based internalization, a cluster of acidic amino acids, and Ser and Tyr phosphorylation motifs, suggesting that DCL-1 CP mediates not only endocytosis and late endosome targeting but also signaling. DCL-1 may be another cell/matrix adhesion receptor integrated in cell adhesion complexes and that DCL-1 dysfunction may affect APC adhesion and migration, causing suppression of APC function.
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TMPY-02221 | Beta-amyloid 42/Beta-APP42 Protein, Human, Recombinant (His & GST) | Human | E. coli | ||
Amyloid precursor protein (APP) is a type I transmembrane protein expressed in many tissues and concentrated in the synapses of neurons, and is suggested as a regulator of synapse formation and neural plasticity. APP can be processed by two different proteolytic pathways. In one pathway, APP is cleaved by β- and γ-secretase to produce the amyloid-β-protein (Aβ, Abeta, beta-amyloid) which is the principal component of the amyloid plaques, the major pathological hallmark of Alzheimer’s disease (AD), while in the other pathway, α-secretase is involved in the cleavage of APP whose product exerts antiamyloidogenic effect and prevention of the Aβ peptide formation. The aberrant accumulation of aggregated beta-amyloid peptides (Abeta) as plaques is a hallmark of AD neuropathology and reduction of Abeta has become a leading direction of emerging experimental therapies for the disease. Besides this pathological function of Abeta, recently published data reveal that Abeta also has an essential physiological role in lipid homeostasis. Cholesterol increases Abeta production, and conversely A beta production causes a decrease in cholesterol synthesis. Abeta may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level, but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. Abeta-induced dysfunction of inhibitory interneurons likely increases synchrony among excitatory principal cells and contributes to the destabilization of neuronal networks. There is evidence that beta-amyloid can impair blood vessel function. Vascular beta-amyloid deposition, also known as cerebral amyloid angiopathy, is associated with vascular dysfunction in animal and human studies. Alzheimer disease is associated with morphological changes in capillary networks, and soluble beta-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli.
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TMPY-02622 | Aldolase B Protein, Human, Recombinant (GST) | Human | E. coli | ||
The aldolase family members involved in metabolism and glycolysis are present in three isoforms: ALDOA, ALDOB, and ALDOC. Aldolases are differentially expressed in human tissues, and aberrant expression has been observed in several human diseases and cancer types. Via GATA6, metastatic cells in the liver upregulate the enzyme aldolase B (ALDOB), which enhances fructose metabolism and provides fuel for major pathways of central carbon metabolism during tumor cell proliferation. Targeting ALDOB or reducing dietary fructose significantly reduces liver metastatic growth but has little effect on the primary tumor. Hereditary fructose intolerance (HFI) is an autosomal recessive disorder caused by aldolase B (ALDOB) deficiency resulting in an inability to metabolize fructose. The toxic accumulation of intermediate fructose-1-phosphate causes multiple metabolic disturbances, including postprandial hypoglycemia, lactic acidosis, electrolyte disturbance, and liver/kidney dysfunction.
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TMPJ-01034 | TIM Protein, Human, Recombinant (His) | Human | E. coli | ||
Triose-phosphate isomerase, also named Triose-phosphate isomerase, TPI and TIM, is an enzyme that catalyzes the reversible interconversion of the triose phosphate isomers dihydroxyacetone phosphate and D-glyceraldehyde 3-phosphate. TPI has been found in nearly every organism searched for the enzyme, including animals such as mammals and insects as well as in fungi, plants, and bacteria. However, some bacteria that do not perform glycolysis, like ureaplasmas, lack TPI. TPI plays an important role in glycolysis and is essential for efficient energy production. TPI deficiency is an autosomal recessive disorder and the most severe clinical disorder of glycolysis. Triose phosphate isomerase deficiency is associated with neonatal jaundice, chronic hemolytic anemia, progressive neuromuscular dysfunction, cardiomyopathy and increased susceptibility to infection and characterized by chronic hemolytic anemia.
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TMPY-02407 | CD302 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
CD302/CLEC13A (C-type lectin domain family 13 member A), also known as C-type lectin receptor DCL-1, is a type I transmembrane C-type lectin DCL-1/CD302. DCL-1 protein was highly conserved among the human, mouse, and rat orthologs. DCL-1 ectodomain contains only one CRD, whereas other type I transmembrane C-type lectins contain more than one domain (e.g. selectins and MMR). DCL-1 CP contains several putative motifs, including a Tyr-based internalization, a cluster of acidic amino acids, and Ser and Tyr phosphorylation motifs, suggesting that DCL-1 CP mediates not only endocytosis and late endosome targeting but also signaling. DCL-1 may be another cell/matrix adhesion receptor integrated in cell adhesion complexes and that DCL-1 dysfunction may affect APC adhesion and migration, causing suppression of APC function.
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TMPH-02526 | Arginase-2/ARG2 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
May play a role in the regulation of extra-urea cycle arginine metabolism and also in down-regulation of nitric oxide synthesis. Extrahepatic arginase functions to regulate L-arginine bioavailability to nitric oxid synthase (NOS). Arginine metabolism is a critical regulator of innate and adaptive immune responses. Seems to be involved in negative regulation of the survival capacity of activated CD4(+) and CD8(+) T cells. May suppress inflammation-related signaling in asthmatic airway epithelium. May contribute to the immune evasion of H.pylori by restricting M1 macrophage activation and polyamine metabolism. May play a role in promoting prenatal immune suppression. Regulates RPS6KB1 signaling, which promotes endothelial cell senescence and inflammation and implicates NOS3/eNOS dysfunction. Can inhibit endothelial autophagy independently of its enzymatic activity implicating mTORC2 signaling. Involved in vascular smooth muscle cell senescence and apoptosis independently of its enzymatic activity.
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TMPY-02110 | Beta-amyloid 40/Beta-APP40 Protein, Human, Recombinant (His & GST) | Human | E. coli | ||
Amyloid precursor protein (APP) is a type I transmembrane protein expressed in many tissues and concentrated in the synapses of neurons, and is suggested as a regulator of synapse formation and neural plasticity. APP can be processed by two different proteolytic pathways. In one pathway, APP is cleaved by β- and γ-secretase to produce the amyloid-β-protein (Aβ, Abeta, beta-amyloid) which is the principal component of the amyloid plaques, the major pathological hallmark of Alzheimer’s disease (AD), while in the other pathway, α-secretase is involved in the cleavage of APP whose product exerts antiamyloidogenic effect and prevention of the Aβ peptide formation. The aberrant accumulation of aggregated beta-amyloid peptides (Abeta) as plaques is a hallmark of AD neuropathology and reduction of Abeta has become a leading direction of emerging experimental therapies for the disease. Besides this pathological function of Abeta, recently published data reveal that Abeta also has an essential physiological role in lipid homeostasis. Cholesterol increases Abeta production, and conversely A beta production causes a decrease in cholesterol synthesis. Abeta may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level, but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. Abeta-induced dysfunction of inhibitory interneurons likely increases synchrony among excitatory principal cells and contributes to the destabilization of neuronal networks. There is evidence that beta-amyloid can impair blood vessel function. Vascular beta-amyloid deposition, also known as cerebral amyloid angiopathy, is associated with vascular dysfunction in animal and human studies. Alzheimer disease is associated with morphological changes in capillary networks, and soluble beta-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli.
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TMPY-03885 | Beta-amyloid 38/Beta-APP38 Protein, Human, Recombinant (aa 672-709, His & GST) | Human | E. coli | ||
Amyloid precursor protein (APP) is a type I transmembrane protein expressed in many tissues and concentrated in the synapses of neurons, and is suggested as a regulator of synapse formation and neural plasticity. APP can be processed by two different proteolytic pathways. In one pathway, APP is cleaved by β- and γ-secretase to produce the amyloid-β-protein (Aβ, Abeta, beta-amyloid) which is the principal component of the amyloid plaques, the major pathological hallmark of Alzheimer’s disease (AD), while in the other pathway, α-secretase is involved in the cleavage of APP whose product exerts antiamyloidogenic effect and prevention of the Aβ peptide formation. The aberrant accumulation of aggregated beta-amyloid peptides (Abeta) as plaques is a hallmark of AD neuropathology and reduction of Abeta has become a leading direction of emerging experimental therapies for the disease. Besides this pathological function of Abeta, recently published data reveal that Abeta also has an essential physiological role in lipid homeostasis. Cholesterol increases Abeta production, and conversely A beta production causes a decrease in cholesterol synthesis. Abeta may be part of a mechanism controlling synaptic activity, acting as a positive regulator presynaptically and a negative regulator postsynaptically. The pathological accumulation of oligomeric Abeta assemblies depresses excitatory transmission at the synaptic level, but also triggers aberrant patterns of neuronal circuit activity and epileptiform discharges at the network level. Abeta-induced dysfunction of inhibitory interneurons likely increases synchrony among excitatory principal cells and contributes to the destabilization of neuronal networks. There is evidence that beta-amyloid can impair blood vessel function. Vascular beta-amyloid deposition, also known as cerebral amyloid angiopathy, is associated with vascular dysfunction in animal and human studies. Alzheimer disease is associated with morphological changes in capillary networks, and soluble beta-amyloid produces abnormal vascular responses to physiological and pharmacological stimuli.
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