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The tumor suppressor WT1 represses and activates transcription. Additionally we are shipping PAWR Antibodies (70) and PAWR Kits (6) and many more products for this protein.
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Authors demonstrate that TRIM21 (show TRIM21 Proteins) 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 (show P2RY12 Proteins) heterodimer internalization/endocytosis is required for beta-arrestin-2 (show ARRB2 Proteins) recruitment to endosomes and up-regulation of Akt (show AKT1 Proteins) signaling; activation of PAR4 but not of P2Y12 (show P2RY12 Proteins) drives internalization of the PAR4-P2Y12 (show P2RY12 Proteins) heterodimer. (PAR4 = protease-activated receptor 4 (show F2RL3 Proteins); P2Y12 (show P2RY12 Proteins) = purinergic receptor P2Y (show P2RY1 Proteins), G-protein coupled, 12 protein; Akt (show AKT1 Proteins) = proto-oncogene (show RAB1A Proteins) protein c-akt (show AKT1 Proteins))
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 (show HSPA5 Proteins) to the cell membrane and subsequent apoptosis of cancer cell
Prostate apoptosis response 4 (PAR4) expression modulates WNT (show WNT2 Proteins) 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 (show HSPA5 Proteins) 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 (show MARK2 Proteins)-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 (show F2RL3 Proteins)/NF-kappaB (show NFKB1 Proteins) in islet beta cell apoptosis and type 2 diabetes.
Par4 (show F2RL3 Proteins), CEBPB (show CEBPB Proteins) and FAK (show PTK2 Proteins) form a senescence signaling pathway, playing roles in modulating cell survival, growth, apoptosis, EMT (show ITK Proteins) and self-renewal
a novel mechanism of apoptosis induction by PAR-4 (show F2RL3 Proteins)/ceramide-enriched exosomes, which may critically contribute to Alzheimer disease.
extracellular Par-4 (show F2RL3 Proteins)/SAC (show ADCY10 Proteins) is systemically functional in inhibition of tumor growth and metastasis progression.
loss of PAR4 (show F2RL3 Proteins) leads to a reduction in the ability of tumour necrosis factor-alpha (show TNF Proteins) to induce apoptosis by increased activation of NF-kappaB (show NFKB1 Proteins)
Antisense knockdown of PAR-4 (show F2RL3 Proteins) or inhibition of ceramide biosynthesis reduced stem cell apoptosis; PAR-4 (show F2RL3 Proteins) overexpression and treatment with ceramide analogs elevated apoptosis.
AATF (show AATF Proteins) is an endogenous antagonist of Par-4 (show F2RL3 Proteins) 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 (show F2RL3 Proteins) is by promoter methylation
direct physical association with ceramide and PAR-4 (show F2RL3 Proteins) regulates the activity of PKCzeta (show PRKCZ Proteins)
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