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The tumor suppressor WT1 represses and activates transcription. Zusätzlich bieten wir Ihnen PAWR Antikörper (70) und PAWR Kits (7) und viele weitere Produktgruppen zu diesem Protein an.
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Authors demonstrate that TRIM21 (zeige TRIM21 Proteine) expression predicts survival in pancreatic cancer patients. This work highlights a novel mechanism of Par-4 regulation, and identifies a novel prognostic marker and potential therapeutic target for pancreatic cancer.
Data suggest that PAR4 and P2Y12 (zeige P2RY12 Proteine) heterodimer internalization/endocytosis is required for beta-arrestin-2 (zeige ARRB2 Proteine) recruitment to endosomes and up-regulation of Akt (zeige AKT1 Proteine) signaling; activation of PAR4 but not of P2Y12 (zeige P2RY12 Proteine) drives internalization of the PAR4-P2Y12 (zeige P2RY12 Proteine) heterodimer. (PAR4 = protease-activated receptor 4 (zeige F2RL3 Proteine); P2Y12 (zeige P2RY12 Proteine) = purinergic receptor P2Y (zeige P2RY1 Proteine), G-protein coupled, 12 protein; Akt (zeige AKT1 Proteine) = proto-oncogene (zeige RAB1A Proteine) protein c-akt (zeige AKT1 Proteine))
In this review, we will focus on the therapeutic perspective of Par-4 with a special reference to its (Par-4) virgin prospect of devastating metastasis control.
in vitro and in vivo upregulation of Par-4 expression is indispensable for the trafficking of GRP78 (zeige HSPA5 Proteine) to the cell membrane and subsequent apoptosis of cancer cell
Prostate apoptosis response 4 (PAR4) expression modulates WNT (zeige WNT2 Proteine) signaling pathways in MCF7 breast cancer cells: A possible mechanism underlying PAR4-mediated docetaxel chemosensitivity.
Decreased PAR4 expression in breast cancer is associated with shorter survival. PAR4 suppresses growth and invasiveness of breast cancer cells.
Authors determined that PAR-4 induces cell apoptosis in response to stimuli, in vitro, but is also involved in the relocation of GRP78 (zeige HSPA5 Proteine) from endoplasmic reticulum to the cell surface of ovarian cancer cell line.
These results suggest that Porphyromonas gingivalis activates PAR4 signaling pathways, leading proMMP9 over-expression and cellular invasion in oral squamous cell carcinoma cells.
PAR1 (zeige MARK2 Proteine)-platelet releasate enhances vasculogenesis more potently than PAR4-platelet releasate, and the enhancements require a cooperation of multiple platelet-derived angiogenic regulators.
A novel long non-coding RNA T-ALL-R-LncR1 knockdown and Par-4 cooperate to induce cellular apoptosis in T-cell acute lymphoblastic leukemia cells.
Findings reveal a novel role for Par-4 (zeige F2RL3 Proteine)/NF-kappaB (zeige NFKB1 Proteine) in islet beta cell apoptosis and type 2 diabetes.
Par4 (zeige F2RL3 Proteine), CEBPB (zeige CEBPB Proteine) and FAK (zeige PTK2 Proteine) form a senescence signaling pathway, playing roles in modulating cell survival, growth, apoptosis, EMT (zeige ITK Proteine) and self-renewal
a novel mechanism of apoptosis induction by PAR-4 (zeige F2RL3 Proteine)/ceramide-enriched exosomes, which may critically contribute to Alzheimer disease.
extracellular Par-4 (zeige F2RL3 Proteine)/SAC (zeige ADCY10 Proteine) is systemically functional in inhibition of tumor growth and metastasis progression.
loss of PAR4 (zeige F2RL3 Proteine) leads to a reduction in the ability of tumour necrosis factor-alpha (zeige TNF Proteine) to induce apoptosis by increased activation of NF-kappaB (zeige NFKB1 Proteine)
Antisense knockdown of PAR-4 (zeige F2RL3 Proteine) or inhibition of ceramide biosynthesis reduced stem cell apoptosis; PAR-4 (zeige F2RL3 Proteine) overexpression and treatment with ceramide analogs elevated apoptosis.
AATF (zeige AATF Proteine) is an endogenous antagonist of Par-4 (zeige F2RL3 Proteine) activity and an effective inhibitor of aberrant amyloid beta 1-42 production and secretion under apoptotic conditions.
Par-4 is directly involved in regulating choline uptake by interacting with CHT1 and by reducing its incorporation on the cell surface
the mechanism for Ras-mediated down-regulation of Par-4 (zeige F2RL3 Proteine) is by promoter methylation
direct physical association with ceramide and PAR-4 (zeige F2RL3 Proteine) regulates the activity of PKCzeta (zeige PRKCZ Proteine)
The tumor suppressor WT1 represses and activates transcription. The protein encoded by this gene is a WT1-interacting protein that itself functions as a transcriptional repressor. It contains a putative leucine zipper domain which interacts with the zinc finger DNA binding domain of WT1. This protein is specifically upregulated during apoptosis of prostate cells.
PRKC, apoptosis, WT1, regulator
, PRKC apoptosis WT1 regulator protein
, PRKC, apoptosis, WT1, regulator like
, WT1-interacting protein
, prostate apoptosis response 4 protein
, prostate apoptosis response protein 4
, prostate apoptosis response protein PAR-4
, prostate apoptosis response-4
, transcriptional repressor PAR4
, Prostate apoptosis response protein 4
, par-4 induced by effectors of apoptosis
, transcriptional repressor Par-4-like protein PAWR