目录号 | 产品详情 | 靶点 | |
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TQ0232 | Histone Methyltransferase | ||
UNC0646 是一种有效的、选择性的同源蛋白赖氨酸甲基转移酶 G9a 和 GLP 抑制剂,IC50分别为 6 和 15 nM,对 G9a/GLP 的选择性比 SETD7、SUV39H2、SETD8 和 PRMT3 高。它降低 MDA-MB-231 细胞中H3K9me2的水平,IC50为 26 nM。 | |||
T7697 | Histone Methyltransferase Autophagy | ||
BIX-01294 是高度选择性的G9a 和GLP 组蛋白甲基转移酶可逆抑制剂。它通过与底物赖氨酸残基 N 端的氨基酸竞争结合来抑制 G9a/GLP,可诱导坏死性凋亡和自噬,具有抗肿瘤活性。 | |||
T4414 | Apoptosis Others Ferroptosis p53 Autophagy | ||
Eprenetapopt (PRIMA-1Met) 是一种在 TP53突变细胞中恢复野生型 p53功能的小分子,可引发肿瘤细胞凋亡,还抑制硒蛋白硫氧还蛋白还原酶 1。 | |||
T8480 | Dehydrogenase Sirtuin HDAC p53 Autophagy | ||
Tenovin-6 Hydrochloride 是 Tenovin-1 的类似物,能抑制二氢乳清酸脱氢酶。它是一种 p53转录活性的激活剂,抑制纯化人 SIRT1、SIRT2 和 SIRT3 蛋白脱乙酰酶活性,IC50分别为 21 μM、10 μM 和 67 μM。 | |||
T8657 | Others | ||
KYP-2047 是一种非常有效的选择性脯氨酰寡肽酶 (POP) 抑制剂。 | |||
T1798 | Mdm2 DNA Alkylator/Crosslinker p53 Autophagy | ||
RITA (NSC-652287) 是 p53-HDM-2相互作用抑制剂,可诱导 DNA-DNA 和 DNA-蛋白质的交联,可与 p53dN 结合,Kd 值为 1.5 nM。 | |||
T36964 | CDK | ||
BML-259 是 CDK5 和 CDK2 的抑制剂,IC50 分别为 64 和 98 nM。 BML-259 可用于癌症和神经退行性疾病治疗的研究。 | |||
T7539 | Apoptosis DNA Alkylation DNA/RNA Synthesis | ||
O6-Benzylguanine 是鸟嘌呤类似物,是 DNA 修复酶 O6 烷基鸟嘌呤DNA 烷基转移酶(MGMT/AGT)抑制剂,可诱导肿瘤细胞凋亡,具有抗肿瘤活性。它作为 AGT 底物,将其苄基转移到 AGT 半胱氨酸残基上,从而不可逆地灭活 AGT 并阻止 DNA 修复。 | |||
T1959 | Histone Methyltransferase Autophagy | ||
BIX-01294 trihydrochloride 是可逆且高度选择性的G9a 和GLP 组蛋白甲基转移酶抑制剂,IC50分别为 1.9 μM 和 0.7 μM。它可诱导坏死性凋亡和自噬,具有抗肿瘤活性。它通过与底物赖氨酸残基 N 端的氨基酸竞争结合来抑制 G9a/GLP。 | |||
T6149 | Apoptosis E1/E2/E3 Enzyme | ||
YH239-EE 是 YH239 的乙酯,是 p53-MDM2 拮抗剂和凋亡诱导剂。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-02228 | p53 Protein, Cynomolgus, Recombinant | Cynomolgus | E. coli | ||
p53, also known as Tp53, is a DNA-binding protein which belongs to the p53 family. It contains transcription activation, DNA-binding, and oligomerization domains. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 (TP53) is a transcription factor whose protein levels and post-translational modification state alter in response to cellular stress (such as DNA damage, hypoxia, spindle damage). Activation of p53 begins through a number of mechanisms including phosphorylation by ATM, ATR, Chk1 and MAPKs. MDM2 is a ubiquitin ligase that binds p53 and targets p53 for proteasomal degradation. Phosphorylation, p14ARF and USP7 prevent MDM2-p53 interactions, leading to an increase in stable p53 tetramers in the cytoplasm. Further modifications such as methylation and acetylation lead to an increase in Tp53 binding to gene specific response elements. Tp53 regulates a large number of genes (>100 genes) that control a number of key tumor suppressing functions such as cell cycle arrest, DNA repair, senescence and apoptosis. Whilst the activation of p53 often leads to apoptosis, p53 inactivation facilitates tumor progression. It is postulated to bind to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Defects in TP53 are a cause of esophageal cancer, Li-Fraumeni syndrome, lung cancer and adrenocortical carcinoma.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPK-01508 | HLA-A*02:01&B2M&P53 WT (HMTEVVRRC) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein. p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPK-01552 | HLA-A*02:01&B2M&P53 R175H (HMTEVVRHC) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPK-01509 | HLA-A*02:01&B2M&P53 WT (HMTEVVRRC) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein. p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPK-01531 | HLA-A*02:01&B2M&P53 R175H (HMTEVVRHC) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPK-01532 | HLA-A*02:01&B2M&P53 R175H (HMTEVVRHC) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPK-01538 | HLA-A*02:01&B2M&P53 WT (HMTEVVRRC) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein. p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPK-01442 | HLA-A*02:01&B2M&P53 WT (HMTEVVRRC) Tetramer Protein, Human, MHC (His & Avi), PE-Labeled | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein. p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPK-01437 | HLA-A*02:01&B2M&P53 R175H (HMTEVVRHC) Tetramer Protein, Human, MHC (His & Avi), PE-Labeled | Human | HEK293 Cells | ||
p53 is a tumor suppressor protein. Under stressful conditions, p53 tightly regulates cell growth by promoting apoptosis and DNA repair. When p53 becomes mutated, it loses its function, resulting in abnormal cell proliferation and tumor progression. Depending on the p53 mutation, it has been shown to form aggregates leading to negative gain of function of the protein.p53 mutant associated aggregation has been observed in several cancer tissues and has been shown to promote tumor growth.
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TMPY-01125 | MDMX Protein, Human, Recombinant (His) | Human | E. coli | ||
MDM4 (MDM4 Regulator Of P53, also known as MDMX) is a Protein Coding gene. This gene encodes a nuclear protein that contains a p53 binding domain at the N-terminus and a RING finger domain at the C-terminus and shows structural similarity to p53-binding protein MDM2. MDM4 is a promising target for cancer therapy, as it is undetectable in most normal adult tissues but often upregulated in cancer cells to dampen p53 tumor-suppressor function. MDM4, an essential negative regulator of the P53 tumor suppressor, is frequently overexpressed in cancer cells that harbor a wild-type P53. MDM4 is a key regulator of p53, whose biological activities depend on both transcriptional activity and transcription-independent mitochondrial functions. MDM4 binds to p53 and blocks its transcriptional activity.
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TMPY-01561 | PIG3 Protein, Human, Recombinant (His) | Human | E. coli | ||
Nutlin-3 variably induces apoptosis and cell cycle arrest in cancer cells while it shows low/absent cytotoxicity in normal cells, Nutlin-3 is a promising anti-cancer agent, which exhibits activity against a variety of cancers, including acute myeloid leukemia (AML). The important role of TP53I3/PIG3 in mediating the apoptotic activity of Nutlin-3 was underlined by knock-down experiments with siRNA specific for TP53I3/PIG3, which resulted in a significant decrease in the pro-apoptotic activity of Nutlin-3.
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TMPH-03264 | p53 Protein, Rat, Recombinant (His) | Rat | E. coli | ||
Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2. However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seems to have an effect on cell-cycle regulation. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1-mediated transcriptional activation of PER2.
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TMPY-03601 | PDRG1 Protein, Human, Recombinant (His) | Human | E. coli | ||
PDRG1, also known as C2orf126, belongs to the prefoldin subunit beta family. It is predominantly expressed in normal testis and exhibits reduced but detectable expression in other organs. PDRG1 may play a role in chaperone-mediated protein folding. PDRG1 is overexpressed in tumors relative to normal tissues. Its expression is upregulated in multiple malignancies including cancers of the colon, rectum, ovary, lung, stomach, breast and uterus when compared to their respective matched normal tissues. Thus PDRG1 is a high-value novel tumor marker that could play a role in cancer development and/or progression.
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TMPH-02574 | p53 Protein, Mouse, Recombinant (His & SUMO) | Mouse | E. coli | ||
Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2. However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis, but seems to have to effect on cell-cycle regulation. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1-mediated transcriptional activation of PER2.
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TMPH-01075 | p53 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
p53 Protein, Human, Recombinant (His & SUMO) is expressed in E. coli expression system with N-6xHis-SUMO tag. The predicted molecular weight is 59.7 kDa and the accession number is P04637.
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TMPJ-00022 | LGALS7 Protein, Human, Recombinant | Human | E. coli | ||
The Galectin family of proteins, with specificity for Nacetyllactosamine containing glycoproteins, consists of beta-galactoside binding lectins containing homologous carbohydrate recognition domains (CRDs).They also possess hemagglutination activity, which is attributable to their bivalent carbohydrate binding properties. Galectins are active both intracellularly and extracellularly. Although they are localized primarily in the cytoplasm and lack a classical signal peptide; they can be secreted by one or more as yet unidentified non-classical secretory pathways. They have diverse effects on many cellular functions including adhesion, migration, polarity, chemotaxis, proliferation, apoptosis, and differentiation. Galectins may play a key role in many pathological states, including autoimmune diseases, allergic reactions, inflammation, tumor cell metastasis, atherosclerosis, and diabetic complications.
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TMPY-05896 | Influenza A H3N2 (A/swine/Thailand/CU-P53/2012) Hemagglutinin/HA Protein (His) | H3N2 | HEK293 Cells | ||
Influenza A H3N2 (A/swine/Thailand/CU-P53/2012) Hemagglutinin/HA Protein (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 57.9 kDa and the accession number is S4TZ09.
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TMPY-02527 | p53R2 Protein, Human, Recombinant (His) | Human | E. coli | ||
Ribonucleoside reductase subunit M2B, also known as RRM2B or p53R2, is an enzyme belonging to the iron-dependent ribonucleotide reductase (RNR) enzyme family which is essential for DNA synthesis. Ribonucleotide reductase (RNR) is an enzyme that catalyzes the formation of deoxyribonucleotides from ribonucleotides and plays a critical role in regulating the total rate of DNA synthesis so that DNA to cell mass is maintained at a constant ratio during cell division and DNA repair. RRM2B is a phosphorylated protein. It is hypothesized that RRM2B activity can be regulated at the posttranslational level in response to DNA damage. RRM2B has previously been shown to be essential for the maintenance of mtDNA copy number and its candidacy for tumor suppression has been evaluated in several mutational analyses of different cancer types. However, the contribution of RRM2B to the DNA damage response has been questioned because its transcriptional induction upon DNA damage is not rapid enough for prompt DNA repair. Instead, ATM-mediated phosphorylation has been suggested to regulate the DNA repair activity of RRM2B posttranslationally. Besides, a defect in RRM2B can induce a mild muscle disease of adult onset through disturbance of mitochondrial homeostasis but that this defect does not appear to be oncogenic.
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TMPH-01520 | HIV-1 (group M, subtype K, isolate 96CM-MP535) Protein Vpr (His & Myc) | HIV-1 | E. coli | ||
HIV-1 (group M, subtype K, isolate 96CM-MP535) Protein Vpr (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 18.8 kDa and the accession number is P0C1P2.
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TMPY-00369 | LY6D Protein, Human, Recombinant (mFc) | Human | HEK293 Cells | ||
LY6D (Lymphocyte Antigen 6 Family Member D) is a Protein Coding gene. It may act as a specification marker at the earliest stage specification of lymphocytes between B- and T-cell development. Marks the earliest stage of B-cell specification. The expression of LY6D is induced in MCF10A cells by X-ray irradiation. The induction of LY6D expression is triggered through a pathway regulated by ATM, CHK2, and p53. This method is a new Ab-directed proteomic strategy for the analysis of membrane proteins and applies to various biological phenomena in situations in which both target molecule-expressing cells and nonexpressing cells are available. Diseases associated with LY6D include Alzheimer's Disease 16 and Inferior Myocardial Infarction.
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TMPY-02030 | CD82 Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
CD82, also known as KAI-1, structurally belongs to tetraspanin family while categorised as metastasis suppressor gene on functional grounds. KAI1/CD82 is localized on cell membrane and form interactions with other tetraspanins, integrins and chemokines which are respectively responsible for cell migration, adhesion and signalling. Downregulation of CD82 expression is associated with the advanced stages of many human cancers and correlates with the acquisition of metastatic potential. Recent studies suggest that complex mechanisms underlie CD82 loss of function, including altered transcriptional regulation, splice variant production and post-translational protein modifications, and indicate a central role for CD82 in controlling metastasis as a 'molecular facilitator'. The loss of KAI1/CD82 expression in invasive and metastatic cancers is due to a complex, epigenetic mechanism that probably involves transcription factors such as NFkappaB, p53, and beta-catenin. A loss of KAI1 expression is also associated with the advanced stages of many human malignancies and results in the acquisition of invasive and metastatic capabilities by tumour cells. Thus, KAI1/CD82 is regarded as a wide-spectrum tumor metastasis suppressor.
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TMPH-01659 | MAGEA4 Protein, Human, Recombinant (A173T, His & Myc) | Human | E. coli | ||
Regulates cell proliferation through the inhibition of cell cycle arrest at the G1 phase. Also negatively regulates p53-mediated apoptosis.
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TMPY-00151 | Alpha SNAP Protein, Human, Recombinant (His) | Human | E. coli | ||
NAPA (NSF Attachment Protein Alpha) is a Protein Coding gene. This gene encodes a member of the soluble NSF attachment protein (SNAP) family. SNAP proteins play a critical role in the docking and fusion of vesicles to target membranes as part of the 20S NSF-SNAP-SNARE complex. NAPA represents an anti-apoptotic protein that promotes resistance to cisplatin in cancer cells by inducing the degradation of the tumor suppressor p53. NAPA overexpression decreased the ubiquitination and degradation of synoviolin and reduced p53 protein level. The combination of cisplatin and knockdown of NAPA represents a novel and attractive strategy to eradicate p53-sensitive cancer cells. NAPA-73 as one of the earliest neuronal markers may reflect a difference between the central and peripheral nervous systems.
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TMPH-01658 | MAGEA4 Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Regulates cell proliferation through the inhibition of cell cycle arrest at the G1 phase. Also negatively regulates p53-mediated apoptosis.
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TMPJ-01211 | EDA2R Protein, Mouse, Recombinant (His) | Mouse | HEK293 Cells | ||
Tumor necrosis factor receptor superfamily member 27, also known as XEDAR and EDA2R, is a type III transmembrane protein of the TNFR superfamily. EDA2R consists of extracellular domain (ECD) with 3 cysteine-rich repeats and a single transmembrane domain but lacks an N-terminal signal peptide. EDA2R is widely expressed, notably in embryonic basal epidermal cells and maturing hair follicles. Even though it does not contain a cytoplasmic death domain, EDA2R can associate with Fas and induce EDA‑A2 dependent apoptosis. Its transcription is directly induced by p53, and it mediated cell death is p53 dependent. it is down‑regulated in breast, colon, and lung cancers, particularly in cases with p53 mutations. It also plays a role in EDA‑A2 induced skeletal muscle degeneration and osteoblast differentiation. Mutations in the EDA gene are associated with the X-linked form of Hypohidrotic Ectodermal Dysplasia (HED), a disease typically characterized by abnormal hair, teeth and sweat glands.
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TMPY-00648 | UNC5A Protein, Human, Recombinant (hFc) | Human | HEK293 Cells | ||
The netrin-1 receptor Uncoordinated Phenotype-5A, or UNC5A, plays an important role in predicting response to DNA damage induced by chemotherapeutic drug and regulating cell death in bladder cancer. Moreover, UNC5A is cumulatively downregulated by the unfolding protein response (UPR) at the transcriptional level in vitro and at the translational level both in vitro and in vivo. Also, UNC5A is a novel transcriptional target of p53 and plays a role in p53-dependent apoptosis. UNC5A Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 58.3 kDa and the accession number is Q6ZN44-1.
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TMPY-00999 | UNC5A Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
The netrin-1 receptor Uncoordinated Phenotype-5A, or UNC5A, plays an important role in predicting response to DNA damage induced by chemotherapeutic drug and regulating cell death in bladder cancer. Moreover, UNC5A is cumulatively downregulated by the unfolding protein response (UPR) at the transcriptional level in vitro and at the translational level both in vitro and in vivo. Also, UNC5A is a novel transcriptional target of p53 and plays a role in p53-dependent apoptosis. UNC5A Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 32.7 kDa and the accession number is Q6ZN44-1.
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TMPH-02221 | TRIM24 Protein, Human, Recombinant (His & SUMO) | Human | E. coli | ||
Transcriptional coactivator that interacts with numerous nuclear receptors and coactivators and modulates the transcription of target genes. Interacts with chromatin depending on histone H3 modifications, having the highest affinity for histone H3 that is both unmodified at 'Lys-4' (H3K4me0) and acetylated at 'Lys-23' (H3K23ac). Has E3 protein-ubiquitin ligase activity. Promotes ubiquitination and proteasomal degradation of p53/TP53. Plays a role in the regulation of cell proliferation and apoptosis, at least in part via its effects on p53/TP53 levels. Up-regulates ligand-dependent transcription activation by AR, GCR/NR3C1, thyroid hormone receptor (TR) and ESR1. Modulates transcription activation by retinoic acid (RA) receptors, including RARA. Plays a role in regulating retinoic acid-dependent proliferation of hepatocytes.
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TMPJ-01278 | SENP8 Protein, Human, Recombinant (His) | Human | E. coli | ||
Sentrin-Specific Protease 8 (SENP8) mediates the reversible covalent modification of proteins by NEDD8. SENP8 catalyzes the full-length NEDD8 to generate its mature form and deconjugation of NEDD8 from targeted proteins such as CUL2 , CUL4A in vivo, or p53. but it does not show activity against ubiquitin or SUMO proteins.
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TMPY-04904 | Zika virus (ZIKV) (strain Zika SPH2015) M/Membrane protein (Fc) | ZIKV | HEK293 Cells | ||
Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. ZIKV has a more selective and larger impact on the expression of genes involved in DNA replication and repair. P53 inhibitors can block the apoptosis induced by ZIKV-M in hNPCs.
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TMPY-02211 | USP5 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Ubiquitin carboxyl-terminal hydrolase 5, also known as Deubiquitinating enzyme 5, Isopeptidase T, Ubiquitin thiolesterase 5, Ubiquitin-specific-processing protease 5, ISOT and USP5, is a member of the peptidase C19 family. USP5 contains 2 UBA domains and one UBP-type zinc finger. The UBP-type zinc finger domain interacts selectively with an unmodified C-terminus of the proximal ubiquitin. Both UBA domains are involved in polyubiquitin recognition. The UBP-type zinc finger domain crystallizes as a dimer linked by a disulfide bond between the Cys-195 residues of both molecules, but there is no evidence that the full-length USP5 exists as a dimer. USP5 cleaves linear and branched multiubiquitin polymers with a marked preference for branched polymers. USP5 is involved in unanchored 'Lys-48'-linked polyubiquitin disassembly. It binds linear and 'Lys-63'-linked polyubiquitin with a lower affinity. Knock-down of USP5 causes the accumulation of p53/TP53 and an increase in p53/TP53 transcriptional activity because the unanchored polyubiquitin that accumulates is able to compete with ubiquitinated p53/TP53 but not with MDM2 for proteasomal recognition.
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TMPH-03269 | COMMD5 Protein, Rat, Recombinant (His & Myc) | Rat | E. coli | ||
May modulate activity of cullin-RING E3 ubiquitin ligase (CRL) complexes. Negatively regulates cell proliferation. Negatively regulates cell cycle G2/M phase transition probably by transactivating p21/CDKN1A through the p53/TP53-independent signaling pathway. Involved in kidney proximal tubule morphogenesis. Down-regulates activation of NF-kappa-B.
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TMPJ-00703 | Gankyrin Protein, Human, Recombinant | Human | E. coli | ||
Gankyrin is a multicatalytic proteinase oncoprotein consists of 7 ankyrin repeats. Gankyrin overexpressed in most hepatocellular carcinomas. Gankyrin is involved in theregulation of the phosphorylation of the retinoblastoma protein by CDK4 to enhance the ubiquitinylation of p53 by MDM2. Gankyrin is also involved in progression of esophageal squamous cell carcinoma. Gankyrin plays an oncogenic role especially in early stages of human epatocarcinogenesis.
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TMPJ-00675 | ZNHIT1 Protein, Human, Recombinant (His) | Human | E. coli | ||
ZNHIT1 belongs to the ZNHIT1 family and contains one HIT-type zinc finger. It can be phosphorylated on Thr by MAPK11 or MAPK14. ZNHIT1 is a component of the chromatin-remodeling SRCAP complex, which is composed of at least SRCAP, DMAP, RUVBL1, RUVBL2, ACTL6A, YEATS4, ACTR6 and ZNHIT1. ZNHIT1 may play a role in p53-mediated apoptosis induction.
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TMPJ-00697 | NOL3 Protein, Human, Recombinant (GST) | Human | E. coli | ||
Nucleolar Protein 3 is encoded by NOL3 gene; multiple transcript variants encoding different isoforms have been found for this gene. So far, Nucleolar protein 3 has show to have two Isoforms. Isoform 1 may be involved in RNA splicing.Isoform 2 may inhibit apoptosis.It has been shown to down-regulate the enzyme activities of caspase 2, caspase 8 and tumor protein p53.
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TMPJ-00571 | UBE2D3 Protein, Human, Recombinant | Human | E. coli | ||
UBE2D3 is an enzyme that belongs to the ubiquitin-conjugating enzyme family. Ubiquitination involves at least three classes of enzymes: ubiquitin-activating enzymes, or E1s, ubiquitin-conjugating enzymes, or E2s, and ubiquitin-protein ligases, or E3s. This enzyme functions in the ubiquitination of the tumor-suppressor protein p53, which is induced by an E3 ubiquitin-protein ligase.
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TMPY-03976 | EEF1E1 Protein, Human, Recombinant (His) | Human | E. coli | ||
EEF1E1, also known as AIMP3 and p18, is a multifunctional protein that localizes to both the cytoplasm and nucleus. In the cytoplasm, EEF1E1 is an auxiliary component of the macromolecular aminoacyl-tRNA synthase complex. It is comprised of a bifunctional glutamyl-prolyl-tRNA synthase, the monospecific isoleucyl, leucyl, glutaminyl, methionyl, lysyl, arginyl and aspartyl-tRNA synthases, and three auxiliary proteins, EEF1E1/p18, AIMP2/p38 and AIMP1/p43. EEF1E1 also plays a positive role in ATM/ATR-mediated p53 activation.
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TMPY-02135 | S100A16 Protein, Human, Recombinant | Human | E. coli | ||
S100A16 is a member of S100 protein superfamily that carries calcium-binding EF-hand motifs. S100 proteins are cell- and tissue-specific and are involved in many intra- and extracellular processes through interacting with specific target proteins. S100A16 expression was found to be astrocyte-specific. The S100A16 protein was found to accumulate within nucleoli and to translocate to the cytoplasm in response to Ca(2+) stimulation. The homodimeric structure of human S100A16 in the apo state has been obtained both in the solid state and in solution, resulting in good agreement between the structures with the exception of two loop regions. The homodimeric solution structure of human S100A16 was also calculated in the calcium(II)-bound form. Differently from most S100 proteins, the conformational rearrangement upon calcium binding is minor. Immunoprecipitation analysis revealed that S100A16 could physically interact with tumor suppressor protein p53, also a known inhibitor of adipogenesis. Overexpression or RNA interference-initiated reduction of S100A16 led to the inhibition or activation of the expression of p53-responsive genes, respectively. S100A16 protein is a novel adipogenesis-promoting factor and that increased expression of S100A16 in 3T3-L1 adipocytes can have a negative impact on insulin sensitivity.
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TMPH-02549 | FHIT Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Possesses dinucleoside triphosphate hydrolase activity. Cleaves P(1)-P(3)-bis(5'-adenosyl) triphosphate (Ap3A) to yield AMP and ADP. Can also hydrolyze P(1)-P(4)-bis(5'-adenosyl) tetraphosphate (Ap4A), but has extremely low activity with ATP. Exhibits adenylylsulfatase activity, hydrolyzing adenosine 5'-phosphosulfate to yield AMP and sulfate. Exhibits adenosine 5'-monophosphoramidase activity, hydrolyzing purine nucleotide phosphoramidates with a single phosphate group such as adenosine 5'monophosphoramidate (AMP-NH2) to yield AMP and NH2. Exhibits adenylylsulfate-ammonia adenylyltransferase, catalyzing the ammonolysis of adenosine 5'-phosphosulfate resulting in the formation of adenosine 5'-phosphoramidate. Also catalyzes the ammonolysis of adenosine 5-phosphorofluoridate and diadenosine triphosphate. Modulates transcriptional activation by CTNNB1 and thereby contributes to regulate the expression of genes essential for cell proliferation and survival, such as CCND1 and BIRC5. Plays a role in the induction of apoptosis via SRC and AKT1 signaling pathways. Inhibits MDM2-mediated proteasomal degradation of p53/TP53 and thereby plays a role in p53/TP53-mediated apoptosis. Induction of apoptosis depends on the ability of FHIT to bind P(1)-P(3)-bis(5'-adenosyl) triphosphate or related compounds, but does not require its catalytic activity. Functions as tumor suppressor.
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TMPJ-00464 | APE Protein, Human, Recombinant | Human | E. coli | ||
Apurinic-Apyrimidinic Endonuclease 1 (APE1) is required for efficient DNA base excision repair. When the DNA glycosylase remove the damaged bases, APE1 cleaves the AP site to allow resynthesis and ligation to complete repair. APE1 stimulates the DNA binding activity of many transcription factors, which participate in cancer promotion and progression. APE1 regulates the redox state of multiple transcription factors, such as c-Jun, c-Fos, NF-kB, p53. APEN is also involved in calcium-dependent down-regulation of PTH expression.
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TMPY-04768 | PRPS2 Protein, Human, Recombinant (His) | Human | E. coli | ||
PRPS2, a subset of PRS, is reported to be a potential protein associated with Sertoli-cell only syndrome. PRPS2 expression correlates with Sertoli-cell only syndrome and inhibits the apoptosis of TM4 Sertoli cells via the p53/Bcl-2/caspases signaling pathway. The gene for PRS II (PRPS2) is located at a different region of the X chromosome, namely Xpter-a21. The promoter region of the human PRPS2 gene was also GC-rich and contained a TATA-like sequence, four Sp1 binding sites and a homopyrimidine stretch.
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TMPJ-01456 | Mucin-17/MUC17 Protein, Human, Recombinant (His) | Human | HEK293 Cells | ||
Mucins are key components of the mucosal barrier in the stomach that protects epithelia from carcinogenic effects of chronic inflammation. Analysis of The Cancer Genome Atlas database indicated that mucin17 (MUC17) was more highly expressed in gastric cancer (GC) specimens, with favourable prognosis for patients. And that p38 signalling is a key factor involved in MUC17-mediated inhibition of GC cell proliferation and protection against inflammatory stimulation, MUC17 upregulates the expression of MYH9 and p53, and activates the p38 pathway in GC cells through RhoA signalling.
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TMPY-02651 | p63 Protein, Human, Recombinant (His & GST) | Human | Baculovirus Insect Cells | ||
Tumor protein p63 is a protein also known as transformation-related protein 63, TP63, and p63. Tumor protein p63 / p63 is a member of the p53 family of transcription factors whose members P53, p63, and p73 have similar features in their gene structures and functions. An animal model, p63-/- mice has been useful in difining the role p63 plays in the development and maintenance of stratified epithelial tissues. This p63 encoding protein p63 has a dramatic impact on replenishment of cutaneous epithelial stem cells and on ovarian germ cell survival. Although these two fundamental roles of p63 attest to its powerful place in development, its other functions, specifically the apparent capacity of p63, is to supervise the emergence of new cell populations in the breast, prostate, cervix, and upper reproductive tract. P63-/- mice have several development defects which include the lack of limbs and other tissues, such as teeth and mammary glands, which develop as a result of interactions between mesenchyme and epithelium. Mutations in this protein are associated with ectodermal dysplasia, and cleft lip / palate syndrome 3, ADULT syndrome (acro-dermato-ungual-lacrimal-tooth), limb-mammary syndrome, et al.
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TMPH-01552 | IRF1 Protein, Human, Recombinant (GST & His) | Human | Baculovirus Insect Cells | ||
Transcriptional regulator which displays a remarkable functional diversity in the regulation of cellular responses. Regulates transcription of IFN and IFN-inducible genes, host response to viral and bacterial infections, regulation of many genes expressed during hematopoiesis, inflammation, immune responses and cell proliferation and differentiation, regulation of the cell cycle and induction of growth arrest and programmed cell death following DNA damage. Stimulates both innate and acquired immune responses through the activation of specific target genes and can act as a transcriptional activator and repressor regulating target genes by binding to an interferon-stimulated response element (ISRE) in their promoters. Competes with the transcriptional repressor ZBED2 for binding to a common consensus sequence in gene promoters. Its target genes for transcriptional activation activity include: genes involved in anti-viral response, such as IFN-alpha/beta, DDX58/RIG-I, TNFSF10/TRAIL, ZBP1, OAS1/2, PIAS1/GBP, EIF2AK2/PKR and RSAD2/viperin; antibacterial response, such as NOS2/INOS; anti-proliferative response, such as p53/TP53, LOX and CDKN1A; apoptosis, such as BBC3/PUMA, CASP1, CASP7 and CASP8; immune response, such as IL7, IL12A/B and IL15, PTGS2/COX2 and CYBB; DNA damage responses and DNA repair, such as POLQ/POLH; MHC class I expression, such as TAP1, PSMB9/LMP2, PSME1/PA28A, PSME2/PA28B and B2M and MHC class II expression, such as CIITA; metabolic enzymes, such as ACOD1/IRG1. Represses genes involved in anti-proliferative response, such as BIRC5/survivin, CCNB1, CCNE1, CDK1, CDK2 and CDK4 and in immune response, such as FOXP3, IL4, ANXA2 and TLR4. Stimulates p53/TP53-dependent transcription through enhanced recruitment of EP300 leading to increased acetylation of p53/TP53. Plays an important role in immune response directly affecting NK maturation and activity, macrophage production of IL12, Th1 development and maturation of CD8+ T-cells. Also implicated in the differentiation and maturation of dendritic cells and in the suppression of regulatory T (Treg) cells development. Acts as a tumor suppressor and plays a role not only in antagonism of tumor cell growth but also in stimulating an immune response against tumor cells.
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TMPJ-00999 | UBE2D1 Protein, Human, Recombinant (GST) | Human | E. coli | ||
Ubiquitin-conjugating enzyme E2 D1(UBE2D1)belongs to the ubiquitin-conjugating enzyme family. Ubiquitination involves at least three classes of enzymes: ubiquitin-activating enzymes, or E1s, ubiquitin-conjugating enzymes, or E2s, and ubiquitin-protein ligases, or E3s. This enzyme is closely related to a stimulator of iron transport (SFT), and is up-regulated in hereditary hemochromatosis. It also functions in the ubiquitination of the tumor-suppressor protein p53 and the hypoxia-inducible transcription factor HIF1alpha by interacting with the E1 ubiquitin-activating enzyme and the E3 ubiquitin-protein ligases.
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TMPY-03443 | NDRG1 Protein, Human, Recombinant (His) | Human | E. coli | ||
NDRG1 gene is a member of the N-Myc downregulated gene family which belongs to the alpha/beta hydrolase superfamily. NDRG1 is a cytoplasmic protein involved in stress responses, hormone responses, cell growth, and differentiation. NDRG1 is necessary for p53-mediated caspase activation and apoptosis. Mutations in the NDRG1 gene are a cause of Charcot-Marie-Tooth disease type 4D, and expression of this gene may be a prognostic indicator for several types of cancer. NDRG1 is a stress-responsive protein involved in hormone responses, cell growth, and differentiation. It acts as a tumor suppressor in many cell types.
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TMPY-03658 | ETHE1 Protein, Human, Recombinant (His) | Human | E. coli | ||
ETHE1, also known as HSCO, is a sulfur dioxygenase that localizes within the mitochondrial matrix. ETHE1 probably plays an important role in metabolic homeostasis in mitochondria. It may also function as a nuclear-cytoplasmic shuttling protein that binds transcription factor RELA/NFKB3 in the nucleus and exports it to the cytoplasm. ETHE1 can suppresses p53-induced apoptosis by preventing nuclear localization of RELA. Mutations in ETHE1 gene result in ethylmalonic encephalopathy. Ethylmalonic encephalopathy is an autosomal recessive, invariably fatal disorder characterized by early-onset encephalopathy, microangiopathy, chronic diarrhea, defective cytochrome c oxidase (COX) in muscle and brain, high concentrations of C4 and C5 acylcarnitines in blood and high excretion of ethylmalonic acid in urine.
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TMPY-02150 | GADD45A Protein, Human, Recombinant (His & GST) | Human | Baculovirus Insect Cells | ||
GADD45A is a member of the GADD45 Family, and has been found to associate with several cytoplasmic and nuclear factors and has been implicated in several cellular functions, including MAPK signaling, cell cycle regulation, DNA repair and genomic stability, apoptosis, and immune responses. The GADD45 Family of genes is rapidly induced by different stressors, including differentiation-inducing cytokines, and there is a large body of evidence that their cognate proteins are key players in cellular stress responses. GADD45A protein has been reported to interact with multiple important cellular proteins, including Cdc2 protein kinase, proliferating cell nuclear antigen (PCNA), p21Waf1/Cip1 protein, core histone protein and MTK/MEKK4, an up-stream activator of the JNK/SAPK pathway, indicating that GADD45A may play important roles in the control of cell cycle checkpoint, DNA repair process, and signaling transduction. GADD45A expression in response to genotoxic stress illustrates a more complex scenario, wherein transcriptional changes operate in concert with mRNA turnover and translational regulation. GADD45A was the first stress-inducible gene determined to be up-regulated by p53 and is also a target for the p53 homologues, p63 and p73. The decreased GADD45A expression is also considered a survival mechanism, as cancer cells without this control can evade the apoptotic pathway leading to increased tumourigenesis. As GADD45A is an essential component of many metabolic pathways that control proliferating cancer cells, it presents itself as an emerging drug target worthy of further investigation.
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TMPJ-00696 | NOL3 Protein, Human, Recombinant | Human | E. coli | ||
Nucleolar protein 3 is encoded by NOL3 gene. Multiple transcript variants encoding different isoforms have been found for this gene. So far, Nucleolar protein 3 has show to have two Isoforms. Isoform 1 may be involved in RNA splicing. Isoform 2 functions as an apoptosis repressor that blocks multiple modes of cell death. It inhibits extrinsic apoptotic pathways through two different ways. Firstly, it by interacting with FAS and FADD upon FAS activation blocking death-inducing signaling complex (DISC) assembly. Secondly by interacting with CASP8 in a mitochondria localization- and phosphorylation-dependent manner, limiting the amount of soluble CASP8 available for DISC-mediated activation. It has been shown to down-regulate the enzyme activities of caspase 2, caspase 8 and tumor protein p53.
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TMPY-04550 | JNK2 Protein, Human, Recombinant (His) | Human | Baculovirus Insect Cells | ||
Mitogen-activated protein kinase 9 (MAPK9), also well known as c-Jun N-terminal kinase (JNK2), is a member of the MAP kinase subfamily belonging to the protein kinase superfamily. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating some transcription factors, such as c-Jun and ATF2. The crystal structure of human JNK2 complexed with an indazole inhibitor by applying a high-throughput protein engineering and surface-site mutagenesis approach. A novel conformation of the activation loop is observed, which is not compatible with its phosphorylation by upstream kinases. This activation inhibitory conformation of JNK2 is stabilized by the MAP kinase insert that interacts with the activation loop in an induced-fit manner. It suggests that the MAP kinase insert of JNK2 plays a role in the regulation of JNK2 activation, possibly by interacting with intracellular binding partners. JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation, and suggests that JNK2 is a negative regulator of cellular proliferation in multiple cell types. JNK2 prevents replicative stress by coordinating cell cycle progression and DNA damage repair mechanisms. JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. JNK2 negatively regulates antigen-specific CD8+ T cell expansion and effector function, and thus selectively blocking JNK2 in CD8+ T cells may potentially enhance the anti-tumor immune response. Lack of JNK2 expression was associated with higher tumor aneuploidy and reduced DNA damage response. Additionally, the JNK2 protein could be a novel therapeutic target in dry eye disease and may provide a novel target for the prevention of vascular disease and atherosclerosis.
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