目录号 | 产品详情 | 靶点 | |
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T22434 | Others | ||
Super-TDU, an inhibitory peptide, targets YAP-TEADs interaction. | |||
T83951 | |||
TM2 TEAD抑制剂是一种有效并且可逆的TEA领域转录因子抑制剂(IC50为TEAD4自动棕榈酰化和TEAD2棕榈酰化分别为38 nM和156 nM)。它抑制TEAD-YAP的结合和转录活性。TM2 TEAD抑制剂在YAP依赖型癌症细胞中,无论是单独使用还是与MEK抑制剂联合使用,都显示出强大的抗增殖效果。同时抑制体外YAP依赖的肝脏类器官生长。 | |||
T81056 | YAP | ||
SWTX-143,一新型共价YAP/TAZ-TEAD 抑制剂,能结合四种TEAD亚型的棕榈酰化口袋。SWTX-143特异性、不可逆地抑制YAP/TAZ-TEAD转录活性,表现出抗肿瘤活性。 | |||
TP1383 | |||
Super-TDU (1-31) is a peptide of Super-TDU, which is an inhibitor of YAP-TEADs, shows potent anti-tumor activity. | |||
T82165 | AMPK | ||
HTH-02-006,一种NUAK2抑制剂(IC50 = 126 nM),能够降低HuCCT-1细胞中磷酸化MYPT1水平,并抑制YAP驱动的细胞增殖、肝肿大和肿瘤发生,同时具备抗纤维化保护效果。 | |||
T76005 | |||
Super-TDU (1-31) 是 Super-TDU 的肽片段。Super-TDU (1-31) 是 YAP-TEAD 复合物的抑制剂。Super-TDU 在胃癌小鼠模型中显示出有效的抗肿瘤活性并抑制肿瘤生长。 | |||
T83938 | |||
TAT-PDHPS1是一种针对Yes-associated protein (YAP) 信号的肽抑制剂。它由内源性肽PDHPS1和能穿透细胞的肽序列TAT组成。PDHPS1与蛋白磷酸酶2磷酸酶激活因子(PTPA)结合, 激活蛋白磷酸酶2A (PP2A)。该激活促进YAP的磷酸化和抑制YAP靶向基因的表达。TAT-PDHPS1能够抑制体外卵巢癌细胞的增殖和小鼠皮下异种移植肿瘤模型中的卵巢肿瘤生长。 | |||
T78558 | |||
GNE-7883是一款泛TEAD抑制剂,有效阻止细胞增殖。该化合物透过抑制YAP/TAZ的激活,克服了多个临床前模型对KRAS G12C抑制剂的抗药性问题。GNE-7883适用于针对YAP/TAZ依赖型肿瘤的研究。 | |||
T76005L | |||
Super-TDU (1-31) TFA 是 Super-TDU 的肽片段。Super-TDU (1-31) TFA 是YAP-TEAD 复合物的抑制剂。Super-TDU TFA 在胃癌小鼠模型中显示出有效的抗肿瘤活性并抑制肿瘤生长。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPH-00005 | YAP1 Protein, Human, Recombinant (Isoform 9, His) | Human | Yeast | ||
YAP1 Protein, Human, Recombinant (Isoform 9, His) is expressed in Yeast with C-terminal 6xHis tag. The predicted molecular weight is 56.4 kDa. Accession number: P46937-9
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TMPH-03764 | YAP1 Protein, Human, Recombinant (His) | Human | Yeast | ||
Transcriptional regulator which can act both as a coactivator and a corepressor and is the critical downstream regulatory target in the Hippo signaling pathway that plays a pivotal role in organ size control and tumor suppression by restricting proliferation and promoting apoptosis. The core of this pathway is composed of a kinase cascade wherein STK3/MST2 and STK4/MST1, in complex with its regulatory protein SAV1, phosphorylates and activates LATS1/2 in complex with its regulatory protein MOB1, which in turn phosphorylates and inactivates YAP1 oncoprotein and WWTR1/TAZ. Plays a key role in tissue tension and 3D tissue shape by regulating cortical actomyosin network formation. Acts via ARHGAP18, a Rho GTPase activating protein that suppresses F-actin polymerization. Plays a key role in controlling cell proliferation in response to cell contact. Phosphorylation of YAP1 by LATS1/2 inhibits its translocation into the nucleus to regulate cellular genes important for cell proliferation, cell death, and cell migration. The presence of TEAD transcription factors are required for it to stimulate gene expression, cell growth, anchorage-independent growth, and epithelial mesenchymal transition (EMT) induction. Suppresses ciliogenesis via acting as a transcriptional corepressor of the TEAD4 target genes AURKA and PLK1. In conjunction with WWTR1, involved in the regulation of TGFB1-dependent SMAD2 and SMAD3 nuclear accumulation.; Activates the C-terminal fragment (CTF) of ERBB4 (isoform 3).; Activates the C-terminal fragment (CTF) of ERBB4 (isoform 3).
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TMPY-04398 | MST1 Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
Dysregulation of MST1/STK4, a key kinase component of the Hippo-YAP pathway, is linked to the etiology of many cancers with poor prognosis. STK4/Hippo pathway may have important therapeutic implications for cancer. The tumor suppressor serine/threonine-protein kinase 4 (STK4) differentially regulates TLR3/4/9-mediated inflammatory responses in macrophages and thereby is protective against chronic inflammation-associated Hepatocellular carcinoma (HCC). STK4 has potential as a diagnostic biomarker and therapeutic target for inflammation-induced HCC.
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TMPH-03208 | IL-6 Protein, Rabbit, Recombinant (His) | Rabbit | Yeast | ||
Cytokine with a wide variety of biological functions in immunity, tissue regeneration, and metabolism. Binds to IL6R, then the complex associates to the signaling subunit IL6ST/gp130 to trigger the intracellular IL6-signaling pathway. The interaction with the membrane-bound IL6R and IL6ST stimulates 'classic signaling', whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells.; IL6 is a potent inducer of the acute phase response. Rapid production of IL6 contributes to host defense during infection and tissue injury, but excessive IL6 synthesis is involved in disease pathology. In the innate immune response, is synthesized by myeloid cells, such as macrophages and dendritic cells, upon recognition of pathogens through toll-like receptors (TLRs) at the site of infection or tissue injury. In the adaptive immune response, is required for the differentiation of B cells into immunoglobulin-secreting cells. Plays a major role in the differentiation of CD4(+) T cell subsets. Essential factor for the development of T follicular helper (Tfh) cells that are required for the induction of germinal-center formation. Required to drive naive CD4(+) T cells to the Th17 lineage. Also required for proliferation of myeloma cells and the survival of plasmablast cells.; Acts as an essential factor in bone homeostasis and on vessels directly or indirectly by induction of VEGF, resulting in increased angiogenesis activity and vascular permeability. Induces, through 'trans-signaling' and synergistically with IL1B and TNF, the production of VEGF. Involved in metabolic controls, is discharged into the bloodstream after muscle contraction increasing lipolysis and improving insulin resistance. 'Trans-signaling' in central nervous system also regulates energy and glucose homeostasis. Mediates, through GLP-1, crosstalk between insulin-sensitive tissues, intestinal L cells and pancreatic islets to adapt to changes in insulin demand. Also acts as a myokine. Plays a protective role during liver injury, being required for maintenance of tissue regeneration. Also has a pivotal role in iron metabolism by regulating HAMP/hepcidin expression upon inflammation or bacterial infection. Through activation of IL6ST-YAP-NOTCH pathway, induces inflammation-induced epithelial regeneration.
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TMPH-03500 | IL-6 Protein, Sheep, Recombinant (GST) | Sheep | E. coli | ||
Cytokine with a wide variety of biological functions in immunity, tissue regeneration, and metabolism. Binds to IL6R, then the complex associates to the signaling subunit IL6ST/gp130 to trigger the intracellular IL6-signaling pathway. The interaction with the membrane-bound IL6R and IL6ST stimulates 'classic signaling', whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells.; IL6 is a potent inducer of the acute phase response. Rapid production of IL6 contributes to host defense during infection and tissue injury, but excessive IL6 synthesis is involved in disease pathology. In the innate immune response, is synthesized by myeloid cells, such as macrophages and dendritic cells, upon recognition of pathogens through toll-like receptors (TLRs) at the site of infection or tissue injury. In the adaptive immune response, is required for the differentiation of B cells into immunoglobulin-secreting cells. Plays a major role in the differentiation of CD4(+) T cell subsets. Essential factor for the development of T follicular helper (Tfh) cells that are required for the induction of germinal-center formation. Required to drive naive CD4(+) T cells to the Th17 lineage. Also required for proliferation of myeloma cells and the survival of plasmablast cells.; Acts as an essential factor in bone homeostasis and on vessels directly or indirectly by induction of VEGF, resulting in increased angiogenesis activity and vascular permeability. Induces, through 'trans-signaling' and synergistically with IL1B and TNF, the production of VEGF. Involved in metabolic controls, is discharged into the bloodstream after muscle contraction increasing lipolysis and improving insulin resistance. 'Trans-signaling' in central nervous system also regulates energy and glucose homeostasis. Mediates, through GLP-1, crosstalk between insulin-sensitive tissues, intestinal L cells and pancreatic islets to adapt to changes in insulin demand. Also acts as a myokine. Plays a protective role during liver injury, being required for maintenance of tissue regeneration. Also has a pivotal role in iron metabolism by regulating HAMP/hepcidin expression upon inflammation or bacterial infection. Through activation of IL6ST-YAP-NOTCH pathway, induces inflammation-induced epithelial regeneration.
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TMPH-01689 | PLD6 Protein, Human, Recombinant (His) | Human | E. coli | ||
Presents phospholipase and nuclease activities, depending on the different physiological conditions. Interaction with Mitoguardin (MIGA1 or MIGA2) affects the dimer conformation, facilitating the lipase activity over the nuclease activity. Plays a key role in mitochondrial fusion and fission via its phospholipase activity. In its phospholipase role, it uses the mitochondrial lipid cardiolipin as substrate to generate phosphatidate (PA or 1,2-diacyl-sn-glycero-3-phosphate), a second messenger signaling lipid. Production of PA facilitates Mitofusin-mediated fusion, whereas the cleavage of PA by the Lipin family of phosphatases produces diacylgycerol (DAG) which promotes mitochondrial fission. Both Lipin and DAG regulate mitochondrial dynamics and membrane fusion/fission, important processes for adapting mitochondrial metabolism to changes in cell physiology. Mitochondrial fusion enables cells to cope with the increased nucleotide demand during DNA synthesis. Mitochondrial function and dynamics are closely associated with biological processes such as cell growth, proliferation, and differentiation. Mediator of MYC activity, promotes mitochondrial fusion and activates AMPK which in turn inhibits YAP/TAZ, thereby inducing cell growth and proliferation. The endonuclease activity plays a critical role in PIWI-interacting RNA (piRNA) biogenesis during spermatogenesis. Implicated in spermatogenesis and sperm fertility in testicular germ cells, its single strand-specific nuclease activity is critical for the biogenesis/maturation of PIWI-interacting RNA (piRNA). MOV10L1 selectively binds to piRNA precursors and funnels them to the endonuclease that catalyzes the first cleavage step of piRNA processing to generate piRNA intermediate fragments that are subsequently loaded to Piwi proteins. Cleaves either DNA or RNA substrates with similar affinity, producing a 5' phosphate end, in this way it participates in the processing of primary piRNA transcripts. piRNAs provide essential protection against the activity of mobile genetic elements. piRNA-mediated transposon silencing is thus critical for maintaining genome stability, in particular in germline cells when transposons are mobilized as a consequence of wide-spread genomic demethylation. PA may act as signaling molecule in the recognition/transport of the precursor RNAs of primary piRNAs. Interacts with tesmin in testes, suggesting a role in spermatogenesis via association with its interacting partner.
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