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    PAWR pro-apoptotic WT1 regulator [ Homo sapiens (human) ]

    Gene ID: 5074, updated on 4-Jan-2025

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Elevated protease-activated receptor 4 (PAR4) gene expression in Alzheimer's disease predicts cognitive decline.

    Elevated protease-activated receptor 4 (PAR4) gene expression in Alzheimer's disease predicts cognitive decline.
    Winfree RL, Erreger K, Phillips J, Seto M, Wang Y, Schneider JA, Bennett DA, Schrag MS, Hohman TJ, Hamm HE.,

    06/20/2024
    CircTRRAP Knockdown Has Cardioprotective Function in Cardiomyocytes via the Signal Regulation of miR-370-3p/PAWR Axis.

    CircTRRAP Knockdown Has Cardioprotective Function in Cardiomyocytes via the Signal Regulation of miR-370-3p/PAWR Axis.
    Zhang Y, Li Z, Wang J, Chen H, He R, Wu H., Free PMC Article

    03/12/2022
    PAR4-Mediated PI3K/Akt and RhoA/ROCK Signaling Pathways Are Essential for Thrombin-Induced Morphological Changes in MEG-01 Cells.

    PAR4-Mediated PI3K/Akt and RhoA/ROCK Signaling Pathways Are Essential for Thrombin-Induced Morphological Changes in MEG-01 Cells.
    Heo Y, Jeon H, Namkung W., Free PMC Article

    02/5/2022
    Determination of PAR4 numbers on the surface of human platelets: no effect of the single nucleotide polymorphism rs773902.

    Determination of PAR4 numbers on the surface of human platelets: no effect of the single nucleotide polymorphism rs773902.
    Li S, Tarlac V, Christanto RBI, French SL, Hamilton JR.

    01/29/2022
    Regulators of G-protein signaling, RGS2 and RGS4, inhibit protease-activated receptor 4-mediated signaling by forming a complex with the receptor and Galpha in live cells.

    Regulators of G-protein signaling, RGS2 and RGS4, inhibit protease-activated receptor 4-mediated signaling by forming a complex with the receptor and Gα in live cells.
    Kim Y, Ghil S., Free PMC Article

    08/14/2021
    Molecular mechanisms regulating Proteinase-Activated Receptors (PARs).

    Molecular mechanisms regulating Proteinase-Activated Receptors (PARs).
    Chandrabalan A, Ramachandran R.

    07/24/2021
    PAR4 activation involves extracellular loop 3 and transmembrane residue Thr153.

    PAR4 activation involves extracellular loop 3 and transmembrane residue Thr153.
    Han X, Hofmann L, de la Fuente M, Alexander N, Palczewski K, INVENT Consortium, Nieman MT., Free PMC Article

    03/27/2021
    Par-4 mediated Smad4 induction in PDAC cells restores canonical TGF-beta/ Smad4 axis driving the cells towards lethal EMT.

    Par-4 mediated Smad4 induction in PDAC cells restores canonical TGF-β/ Smad4 axis driving the cells towards lethal EMT.
    Mohd Faheem M, Rasool RU, Ahmad SM, Jamwal VL, Chakraborty S, Katoch A, Gandhi SG, Bhagat M, Goswami A.

    10/31/2020
    A Platelet Function Modulator of Thrombin Activation Is Causally Linked to Cardiovascular Disease and Affects PAR4 Receptor Signaling.

    A Platelet Function Modulator of Thrombin Activation Is Causally Linked to Cardiovascular Disease and Affects PAR4 Receptor Signaling.
    Rodriguez BAT, Bhan A, Beswick A, Elwood PC, Niiranen TJ, Salomaa V, FinnGen Study, Trégouët DA, Morange PE, Civelek M, Ben-Shlomo Y, Schlaeger T, Chen MH, Johnson AD., Free PMC Article

    10/24/2020
    Par-4 regulates autophagic cell death in human cancer cells via upregulating p53 and BNIP3.

    Par-4 regulates autophagic cell death in human cancer cells via upregulating p53 and BNIP3.
    Thayyullathil F, Cheratta AR, Pallichankandy S, Subburayan K, Tariq S, Rangnekar VM, Galadari S.

    10/24/2020
    These findings have identified an in vivo antileukemic role for Par-4 through an NF-kappaB-dependent mechanism in TCL1-mediated CLL-like disease progression.

    Par-4 overexpression impedes leukemogenesis in the Eµ-TCL1 leukemia model through downregulation of NF-κB signaling.
    Greene JT, Mani R, Ramaswamy R, Frissora F, Yano M, Zapolnik K, Harrington B, Wasmuth R, Tran M, Mo X, McKenna M, Rangnekar VM, Byrd JC, Bondada S, Muthusamy N., Free PMC Article

    05/16/2020
    In further investigations into the functions and molecular mechanisms of PAR4 in ESCC.

    Quantitative Proteomics Identify the Possible Tumor Suppressive Role of Protease-Activated Receptor-4 in Esophageal Squamous Cell Carcinoma Cells.
    Wang M, An S, Wang D, Ji H, Geng M, Guo X, Wang Z.

    12/21/2019
    These results identify Twist-induced epigenetic silencing of Par-4 as a targetable axis that promotes chemoresistance in recurrent breast cancer.

    Epigenetic silencing of tumor suppressor Par-4 promotes chemoresistance in recurrent breast cancer.
    Mabe NW, Fox DB, Lupo R, Decker AE, Phelps SN, Thompson JW, Alvarez JV., Free PMC Article

    09/14/2019
    These results suggest that PtdIns 4-kinase II beta may be a novel regulator of Par-4 through protein-protein interactions.

    Silencing of type II phosphatidylinositol 4-kinase β stabilizes prostate apoptosis response-4 and induces apoptosis in cancer cells.
    Chaudhry S, Joshi V, Bojjireddy N, Thoh M, Sandur SK, Subrahmanyam G.

    09/7/2019
    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.

    Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K-Akt Inhibition.
    Damrauer JS, Phelps SN, Amuchastegui K, Lupo R, Mabe NW, Walens A, Kroger BR, Alvarez JV., Free PMC Article

    08/3/2019
    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.

    Novel role of prostate apoptosis response-4 tumor suppressor in B-cell chronic lymphocytic leukemia.
    McKenna MK, Noothi SK, Alhakeem SS, Oben KZ, Greene JT, Mani R, Perry KL, Collard JP, Rivas JR, Hildebrandt GC, Fleischman RA, Durbin EB, Byrd JC, Wang C, Muthusamy N, Rangnekar VM, Bondada S., Free PMC Article

    07/20/2019
    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.

    pH-Induced Folding of the Caspase-Cleaved Par-4 Tumor Suppressor: Evidence of Structure Outside of the Coiled Coil Domain.
    Clark AM, Ponniah K, Warden MS, Raitt EM, Yawn AC, Pascal SM., Free PMC Article

    06/1/2019
    siRNA-mediated silencing of endogenous Par-4 unveil reversal of mesenchymal-epithelial transition with diminished E-cadherin expression and invasive pancreatic cancer cells phenotypes.

    Dual role of Par-4 in abrogation of EMT and switching on Mesenchymal to Epithelial Transition (MET) in metastatic pancreatic cancer cells.
    Katoch A, Suklabaidya S, Chakraborty S, Nayak D, Rasool RU, Sharma D, Mukherjee D, Faheem MM, Kumar A, Sharma PR, Senapati S, Kumar LD, Goswami A.

    04/27/2019
    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.

    Protease-activated receptor 4 activity promotes platelet granule release and platelet-leukocyte interactions.
    Rigg RA, Healy LD, Chu TT, Ngo ATP, Mitrugno A, Zilberman-Rudenko J, Aslan JE, Hinds MT, Vecchiarelli LD, Morgan TK, Gruber A, Temple KJ, Lindsley CW, Duvernay MT, Hamm HE, McCarty OJT., Free PMC Article

    03/16/2019
    These findings suggest that PAR4 plays a potential tumor suppressor role in esophageal squamous cell carcinoma cells

    Activation of PAR4 Upregulates p16 through Inhibition of DNMT1 and HDAC2 Expression via MAPK Signals in Esophageal Squamous Cell Carcinoma Cells.
    Wang M, An S, Wang D, Ji H, Guo X, Wang Z., Free PMC Article

    12/29/2018
    we determined that increased miR-17-3P level plays crucial role in CRC cells survival by targeting Par4, contributing to colorectal carcinogenesis.

    miR-17-3P regulates the proliferation and survival of colon cancer cells by targeting Par4.
    Lu D, Tang L, Zhuang Y, Zhao P.

    07/14/2018
    PAR4 is the target of mir-107 in colorectal cancer cells.

    miR-107 Promotes Proliferation and Inhibits Apoptosis of Colon Cancer Cells by Targeting Prostate Apoptosis Response-4 (Par4).
    Liu F, Liu S, Ai F, Zhang D, Xiao Z, Nie X, Fu Y., Free PMC Article

    03/31/2018
    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.

    Cancer-associated fibroblasts promote cancer cell growth through a miR-7-RASSF2-PAR-4 axis in the tumor microenvironment.
    Shen Z, Qin X, Yan M, Li R, Chen G, Zhang J, Chen W., Free PMC Article

    03/10/2018
    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

    Post-translational regulation of the cleaved fragment of Par-4 in ovarian and endometrial cancer cells.
    Brasseur K, Fabi F, Adam P, Parent S, Lessard L, Asselin E., Free PMC Article

    01/13/2018
    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.

    TRIM21 is a novel regulator of Par-4 in colon and pancreatic cancer cells.
    Nguyen JQ, Irby RB., Free PMC Article

    09/23/2017
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