目录号 | 产品详情 | 靶点 | |
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T74817 | |||
JNK3inhibitor-7 是一种有效的口服活性JNK3抑制剂,能穿过血脑屏障,其对JNK3、JNK2、JNK1的IC50值分别为53、973、1039 nM。该化合物表现出显著的神经保护作用,并具备研究阿尔茨海默病(AD)潜力。 | |||
T8661 | JNK | ||
AS601245.2TFA (345987-15-7 free base) (AS601245.2TFA) 是一种可渗透细胞的 JNK 抑制剂(对 hJNK1、hJNK2 和 hJNK3 的 IC50 分别为 150、220 和 70 nM)。 | |||
T9138 | GSK-3 CDK JNK | ||
Indirubin-3′-oxime 是一种有效的细胞周期蛋白依赖性蛋白激酶抑制剂,是 indirubin 的合成衍生物。它可通过激活软骨细胞中的 Wnt/β-catenin 信号来促进身高增长,可能在阿尔茨海默病的神经元凋亡中发挥作用。 | |||
T72714 | JNK | ||
JNK3inhibitor-3(compound 15g)是一种选择性的c-Jun N-terminal kinase3(JNK3)抑制剂,具有良好的血脑屏障穿透性和口服生物利用度。其对JNK1、JNK2和JNK3的IC50分别为147.8 nM、44.0 nM和4.1 nM。在小鼠痴呆模型中,JNK3inhibitor-3能显著改善记忆功能,因此有望作为阿尔茨海默病研究的工具化合物。 | |||
T36260 | |||
Potent and selective p38α and p38β degrader (DC50 < 50 nM). Displays no significant degradation of p38γ, p38δ, JNK1/2 or ERK1/2. Inhibits phosphorylation of MK2 in UV-treated cancer cells and LPS-stimulated bone marrow-derived macrophages (BMDM). Exhibits similar effect to p38α gene knockout in BBL358 cells. Active in vivo. | |||
T74818 | |||
JNK3inhibitor-8是一种高效、选择性且具口服活性的JNK3抑制剂,能穿透血脑屏障。其对JNK3、JNK2、JNK1的IC50值依次为21, 2203, >10000 nM。JNK3inhibitor-8展现出显著的神经保护性能,并具备研究阿尔茨海默病(AD)的可能性。 | |||
T72715 | |||
JNK3inhibitor-4 是一种强效的JNK3抑制剂(IC50=1.0 nM),属于2-芳基-1-嘧啶基-1H-咪唑-5-基乙腈衍生物。该化合物对JNK3表现出高度专一性,对比JNK1(IC50=143.9 nM)和JNK2(IC50=298.2 nM)的选择性显著。此外,JNK3inhibitor-4还具备神经保护特性及良好的血脑屏障透过性预期。 | |||
T10298L2 | p38 MAPK | ||
AMG-548 dihydrochloride is an orally active and selective p38α inhibitor (Ki: 0.5 nM) and shows slightly selective over p38β (Ki: 36 nM) and >1000 fold selective against p38γ/p38δ. It is also extremely potent in the inhibition of whole blood LPS stimulate | |||
T10298 | p38 MAPK | ||
AMG-548 hydrochloride is an orally active and selective p38α inhibitor (Ki: 0.5 nM) and shows slightly selective over p38β (Ki: 36 nM) and >1000 fold selective against p38γ/p38δ. It is also extremely potent in the inhibition of whole blood LPS stimulated TNFα (IC50: 3 nM). | |||
T10298L | p38 MAPK | ||
AMG-548 is an orally active and selective p38α inhibitor (Ki=0.5 nM), shows slightly selective over p38β (Ki=36 nM) and >1000 fold selective against p38γ and p38δ and is also extremely potent in the inhibition of whole blood LPS stimulated TNFα (IC50=3 nM |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04554 | JNK1 Protein, Human, Recombinant (GST) | Human | Baculovirus-Insect Cells | ||
Mitogen-activated protein kinase 8 (MAPK8), also known as JNK1, is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation, and development. The protein kinases JNK1 has been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. It is critically involved in the promotion of diet-induced obesity, metabolic inflammation, and beta-cell dysfunction. The selective deficiency of JNK1 in the murine nervous system is sufficient to suppress diet-induced obesity. Genetic analysis indicates that the effects of JNK1 can be separated from the effects of JNK1 on obesity. JNK1 is a potential pharmacological target for the development of drugs that might be useful for the treatment of metabolic syndrome, and type 2 diabetes. Furthermore, JNK1 plays a major role in hypoxic cellular damage. JNK1 protein might be an attractive target for anti-hypoxic therapy in increasing resistance to many pathological conditions and diseases, leading to the oxygen deficit.
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TMPY-06842 | BMP-4 Protein, Human, Recombinant (E399D) | Human | E. coli | ||
BMP4 (bone morphogenetic protein-4)-directed differentiation of human embryonic stem cells (ESCd). Autophagy is a conserved catabolic process with complicated roles in tumor development. Bone morphogenetic protein 4 (BMP4), a member of the transforming growth factor (TGF-β) family of regulatory proteins, plays a crucial role in human malignancies. BMP4 treatment promoted HCC cells proliferation and induced autophagy. Mechanistic study revealed that the induction of autophagy by BMP4 was mediated through activating the JNK1/Bcl2 pathway. And the JNK1 inhibitor and knockdown of JNK1 could attenuate autophagy induced by BMP4 and eliminated BMP4-promoted HCC cells growth. BMP4 promoted HCC proliferation by autophagy activation through JNK1/Bcl-2 signaling.
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TMPY-04572 | MKK4 Protein, Mouse, Recombinant (His & GST) | Mouse | Baculovirus-Insect Cells | ||
Dual specificity mitogen-activated protein kinase kinase 4, also known as MAP kinase kinase 4, MAPKK4, JNK-activating kinase 1, MAPK/ERK kinase 4, SAPK/ERK kinase 1, c-Jun N-terminal kinase kinase 1, JNKK, and MAP2K4, is a protein that belongs to the protein kinase superfamily, STE Ser/Thr protein kinase family and MAP kinase kinase subfamily. MAP2K4 / JNKK1 is a protein kinase that is a direct activator of MAP kinases in response to various environmental stresses or mitogenic stimuli. MAP2K4 / JNKK1 has been shown to activate MAPK8 / JNK1, MAPK9 / JNK2, and MAPK14 / p38, but not MAPK1 / ERK2 or MAPK3 / ERK1. MAP2K4 / JNKK1 is phosphorylated, and thus activated by MAP3K1 / MEKK. The stress-activated protein kinase (SAPK) pathways represent phosphorylation cascades that convey pro-apoptotic signals. The mitogen-activated protein kinase kinase (MAPKK) homolog MAP2K4 ( MKK4, SEK, JNKK1 ) is a centrally-placed mediator of the SAPK pathways.
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TMPY-00431 | BMP-4 Protein, Mouse, Recombinant (rFc) | Mouse | HEK293 | ||
BMP4 (bone morphogenetic protein-4)-directed differentiation of human embryonic stem cells (ESCd). Autophagy is a conserved catabolic process with complicated roles in tumor development. Bone morphogenetic protein 4 (BMP4), a member of the transforming growth factor (TGF-β) family of regulatory proteins, plays a crucial role in human malignancies. BMP4 treatment promoted HCC cells proliferation and induced autophagy. Mechanistic study revealed that the induction of autophagy by BMP4 was mediated through activating the JNK1/Bcl2 pathway. And the JNK1 inhibitor and knockdown of JNK1 could attenuate autophagy induced by BMP4 and eliminated BMP4-promoted HCC cells growth. BMP4 promoted HCC proliferation by autophagy activation through JNK1/Bcl-2 signaling.
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TMPJ-00928 | Serpin B3 Protein, Human, Recombinant (C-His) | Human | Human Cells | ||
Serpin B3, also known as squamous cell carcinoma antigen-1 (SCCA-1), is a member of the serpin superfamily of serine protease inhibitors. Serpin B3 belongs to the subgroup ovalbumin-related serpins which are involved in the regulation of apoptosis, inflammation, angiogenesis and embryogenesis. It may act as a papain-like cysteine protease inhibitor to modulate the host immune response against tumor cells. It also functions as an inhibitor of UV-induced apoptosis via suppression of the activity of c-Jun NH(2)-terminal kinase (JNK1).
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TMPJ-00929 | Serpin B3 Protein, Human, Recombinant (N-His) | Human | E. coli | ||
Serpin B3, also known as squamous cell carcinoma antigen-1 (SCCA-1), is a member of the serpin superfamily of serine protease inhibitors. Serpin B3 belongs to the subgroup ovalbumin-related serpins which are involved in the regulation of apoptosis, inflammation, angiogenesis and embryogenesis. It may act as a papain-like cysteine protease inhibitor to modulate the host immune response against tumor cells. It also functions as an inhibitor of UV-induced apoptosis via suppression of the activity of c-Jun NH(2)-terminal kinase (JNK1).
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TMPH-02962 | Lyn Protein, Mouse, Recombinant (His & Myc) | Mouse | E. coli | ||
Non-receptor tyrosine-protein kinase that transmits signals from cell surface receptors and plays an important role in the regulation of innate and adaptive immune responses, hematopoiesis, responses to growth factors and cytokines, integrin signaling, but also responses to DNA damage and genotoxic agents. Functions primarily as negative regulator, but can also function as activator, depending on the context. Required for the initiation of the B-cell response, but also for its down-regulation and termination. Plays an important role in the regulation of B-cell differentiation, proliferation, survival and apoptosis, and is important for immune self-tolerance. Acts downstream of several immune receptors, including the B-cell receptor, CD79A, CD79B, CD5, CD19, CD22, FCER1, FCGR2, FCGR1A, TLR2 and TLR4. Plays a role in the inflammatory response to bacterial lipopolysaccharide. Mediates the responses to cytokines and growth factors in hematopoietic progenitors, platelets, erythrocytes, and in mature myeloid cells, such as dendritic cells, neutrophils and eosinophils. Acts downstream of EPOR, KIT, MPL, the chemokine receptor CXCR4, as well as the receptors for IL3, IL5 and CSF2. Plays an important role in integrin signaling. Regulates cell proliferation, survival, differentiation, migration, adhesion, degranulation, and cytokine release. Down-regulates signaling pathways by phosphorylation of immunoreceptor tyrosine-based inhibitory motifs (ITIM), that then serve as binding sites for phosphatases, such as PTPN6/SHP-1, PTPN11/SHP-2 and INPP5D/SHIP-1, that modulate signaling by dephosphorylation of kinases and their substrates. Phosphorylates LIME1 in response to CD22 activation. Phosphorylates BTK, CBL, CD5, CD19, CD72, CD79A, CD79B, CSF2RB, DOK1, HCLS1, LILRB3/PIR-B, MS4A2/FCER1B, SYK and TEC. Promotes phosphorylation of SIRPA, PTPN6/SHP-1, PTPN11/SHP-2 and INPP5D/SHIP-1. Required for rapid phosphorylation of FER in response to FCER1 activation. Mediates KIT phosphorylation. Acts as an effector of EPOR (erythropoietin receptor) in controlling KIT expression and may play a role in erythroid differentiation during the switch between proliferation and maturation. Depending on the context, activates or inhibits several signaling cascades. Regulates phosphatidylinositol 3-kinase activity and AKT1 activation. Regulates activation of the MAP kinase signaling cascade, including activation of MAP2K1/MEK1, MAPK1/ERK2, MAPK3/ERK1, MAPK8/JNK1 and MAPK9/JNK2. Mediates activation of STAT5A and/or STAT5B. Phosphorylates LPXN on 'Tyr-72'. Kinase activity facilitates TLR4-TLR6 heterodimerization and signal initiation. Phosphorylates SCIMP on 'Tyr-96'; this enhances binding of SCIMP to TLR4, promoting the phosphorylation of TLR4, and a selective cytokine response to lipopolysaccharide in macrophages. Phosphorylates CLNK.
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