PRKC, Apoptosis, WT1, Regulator Proteins (PAWR)

Human PRKC, Apoptosis, WT1, Regulator (PAWR) interaction partners

1. Results indicate that residual breast cancer tumor cell survival and recurrence requires circumventing Foxo-driven Par-4 upregulation and suggest that approaches to enforce Par-4 expression may prevent residual cell survival and recurrence.

2. Chronic lymphocytic leukemia (CLL) cells overexpress a well-defined tumor suppressor Par-4, which promotes malignant B-CLL growth and is regulated through B-cell receptor signaling.

3. The results demonstrate pH-dependent folding of cl-Par-4, with high disorder and aggregation at neutral pH, but a largely folded, non-aggregated conformation at acidic pH.

4. siRNA-mediated silencing of endogenous Par-4 unveil reversal of mesenchymal-epithelial transition with diminished E-cadherin expression and invasive pancreatic cancer cells phenotypes.

5. These results indicate PAR4-specific promotion of platelet granule release and platelet-leukocyte aggregate formation and suggest that pharmacological control of PAR4 activity could potentially attenuate platelet granule release or platelet-leukocyte interaction-mediated pathological processes.

6. These findings suggest that PAR4 plays a potential tumor suppressor role in esophageal squamous cell carcinoma cells

7. we determined that increased miR-17-3P level plays crucial role in CRC cells survival by targeting Par4, contributing to colorectal carcinogenesis.

8. PAR4 is the target of mir-107 in colorectal cancer cells.

9. we confirmed that the RASSF2-PAR-4 axis was mainly responsible for miR-7 functions in CAFs using bioinformatics methods. Overexpression of miR-7 in CAFs led to down-regulation of RASSF2, which dramatically decreased the secretion of PAR-4 from CAFs and then enhanced the proliferation and migration of the co-cultured cancer cells.

10. we investigated in the present study the mechanisms regulating the accumulation of a 25kDa cleaved-Par-4 (cl-Par-4) fragment in ovarian and endometrial cancer cell lines

11. Authors demonstrate that TRIM21 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.

12. Data suggest that PAR4 and P2Y12 heterodimer internalization/endocytosis is required for beta-arrestin-2 recruitment to endosomes and up-regulation of Akt signaling; activation of PAR4 but not of P2Y12 drives internalization of the PAR4-P2Y12 heterodimer. (PAR4 = protease-activated receptor 4; P2Y12 = purinergic receptor P2Y, G-protein coupled, 12 protein; Akt = proto-oncogene protein c-akt)

13. 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.

14. in vitro and in vivo upregulation of Par-4 expression is indispensable for the trafficking of GRP78 to the cell membrane and subsequent apoptosis of cancer cell

15. Prostate apoptosis response 4 (PAR4) expression modulates WNT signaling pathways in MCF7 breast cancer cells: A possible mechanism underlying PAR4-mediated docetaxel chemosensitivity.

16. Decreased PAR4 expression in breast cancer is associated with shorter survival. PAR4 suppresses growth and invasiveness of breast cancer cells.

17. Authors determined that PAR-4 induces cell apoptosis in response to stimuli, in vitro, but is also involved in the relocation of GRP78 from endoplasmic reticulum to the cell surface of ovarian cancer cell line.

18. These results suggest that Porphyromonas gingivalis activates PAR4 signaling pathways, leading proMMP9 over-expression and cellular invasion in oral squamous cell carcinoma cells.

19. PAR1-platelet releasate enhances vasculogenesis more potently than PAR4-platelet releasate, and the enhancements require a cooperation of multiple platelet-derived angiogenic regulators.

20. 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.

Mouse (Murine) PRKC, Apoptosis, WT1, Regulator (PAWR) interaction partners

1. Lack of Par-4 increased the expression of p21 and delayed chronic lymphocytic leukemia (CLL) growth in Emu-Tcl1 mice.

2. Induced by endoplasmic reticulum stress Par-4 acts as an important defense mechanism against mycobacterial infection and regulates cancer.

3. Findings reveal a novel role for Par-4/NF-kappaB in islet beta cell apoptosis and type 2 diabetes.

4. Par4, CEBPB and FAK form a senescence signaling pathway, playing roles in modulating cell survival, growth, apoptosis, EMT and self-renewal

5. a novel mechanism of apoptosis induction by PAR-4/ceramide-enriched exosomes, which may critically contribute to Alzheimer disease.

6. extracellular Par-4/SAC is systemically functional in inhibition of tumor growth and metastasis progression.

7. loss of PAR4 leads to a reduction in the ability of tumour necrosis factor-alpha to induce apoptosis by increased activation of NF-kappaB

8. Antisense knockdown of PAR-4 or inhibition of ceramide biosynthesis reduced stem cell apoptosis; PAR-4 overexpression and treatment with ceramide analogs elevated apoptosis.

9. Regulates T cell proliferation and differentiation.

10. AATF is an endogenous antagonist of Par-4 activity and an effective inhibitor of aberrant amyloid beta 1-42 production and secretion under apoptotic conditions.

11. Par-4 is directly involved in regulating choline uptake by interacting with CHT1 and by reducing its incorporation on the cell surface

12. the mechanism for Ras-mediated down-regulation of Par-4 is by promoter methylation

13. direct physical association with ceramide and PAR-4 regulates the activity of PKCzeta

14. Par-4 is identified as a regulatory component in dopamine signaling

15. Determined the first SPRY-domain structure of SSB-2 that adopts a novel fold and contains conserved structural determinants for binding to prostate apoptosis response protein-4 (PAR-4).

16. Results describe a novel isoform of prostate apoptosis response 4 (PAR-4) that co-distributes with F-actin and prevents apoptosis in neural stem cells.

17. Par-4 is a novel and early mediator of renal tubule cell injury following ischemia-reperfusion-induced renal injury and provide a potential target for developing new therapeutic strategies for renal ischemia-reperfusion-induced renal injury

18. examined calcium mobilization in platelets from mice that were wild-type or homozygous null for PAR-4 or P2Y1 receptors, hypothesizing that the loss of PAR-4 or P2Y1 receptors would cause redistribution of its Galphaq proteins to other receptors [PAR-4]

19. The lack of Par-4 dramatically enhances Ras-induced lung carcinoma formation in vivo, acting as a negative regulator of Akt activation.

20. cooperation between Par-4 and PTEN as relevant for the development of prostate cancer and implicate the NF-kappaB pathway as a critical event in prostate tumorigenesis.