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    PHLDA3 pleckstrin homology like domain family A member 3 [ Homo sapiens (human) ]

    Gene ID: 23612, updated on 2-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    PHLDA3 Is an Important Downstream Mediator of p53 in Squamous Cell Carcinogenesis.

    PHLDA3 Is an Important Downstream Mediator of p53 in Squamous Cell Carcinogenesis.
    Saito M, Sada A, Fukuyo M, Aoki K, Okumura K, Tabata Y, Chen Y, Kaneda A, Wakabayashi Y, Ohki R.

    05/14/2022
    PHLDA3 exerts an antitumor function in prostate cancer by down-regulating Wnt/beta-catenin pathway via inhibition of Akt.

    PHLDA3 exerts an antitumor function in prostate cancer by down-regulating Wnt/β-catenin pathway via inhibition of Akt.
    Ma S, Quan P, Yu C, Fan X, Yang S, Jia W, Zhang L, Wang F, Liu F, Yang L, Qin W, Yang X.

    11/22/2021
    Prognostic and predictive value of Pleckstrin homology-like domain, family A family members in breast cancer.

    Prognostic and predictive value of Pleckstrin homology-like domain, family A family members in breast cancer.
    R Mangone F, Av Valoyes M, G do Nascimento R, Pf Conceição M, R Bastos D, C Pavanelli A, C Soares I, S de Mello E, Nonogaki S, Ab de T Osório C, A Nagai M.

    10/16/2021
    Novel Role for Pleckstrin Homology-Like Domain Family A, Member 3 in the Regulation of Pathological Cardiac Hypertrophy.

    Novel Role for Pleckstrin Homology-Like Domain Family A, Member 3 in the Regulation of Pathological Cardiac Hypertrophy.
    Liu J, Liu X, Hui X, Cai L, Li X, Yang Y, Shu S, Wang F, Xia H, Li S., Free PMC Article

    11/21/2020
    Phlda3 regulates beta cell survival during stress.

    Phlda3 regulates beta cell survival during stress.
    Bensellam M, Chan JY, Lee K, Joglekar MV, Hardikar AA, Loudovaris T, Thomas HE, Jonas JC, Laybutt DR., Free PMC Article

    10/24/2020
    Recommendation of long-term and systemic management according to the risk factors in rectal NETs patients.

    Recommendation of long-term and systemic management according to the risk factors in rectal NETs patients.
    Kojima M, Chen Y, Ikeda K, Tsukada Y, Takahashi D, Kawano S, Amemiya K, Ito M, Ohki R, Ochiai A., Free PMC Article

    09/12/2020
    although iPSCs and ESCs share lots of common features, we did not find that PHLDA3 is important to ES cell differentiation.

    PHLDA3 impedes somatic cell reprogramming by activating Akt-GSK3β pathway.
    Qiao M, Wu M, Shi R, Hu W., Free PMC Article

    12/22/2018
    Low PHLDA3 expression in ESCC may be predictive of tumor recurrence suggesting that Akt activation may be a therapeutic target in ESCCs

    Low PHLDA3 expression in oesophageal squamous cell carcinomas is associated with poor prognosis.
    Muroi H, Nakajima M, Satomura H, Takahashi M, Yamaguchi S, Sasaki K, Yokobori T, Miyazaki T, Kuwano H, Kato H.

    04/11/2015
    Results indicate that tumor suppressor PHLDA3-mediated pathway is important in the development of pancreatic neuroendocrine tumors (PanNETs).

    PHLDA3 is a novel tumor suppressor of pancreatic neuroendocrine tumors.
    Ohki R, Saito K, Chen Y, Kawase T, Hiraoka N, Saigawa R, Minegishi M, Aita Y, Yanai G, Shimizu H, Yachida S, Sakata N, Doi R, Kosuge T, Shimada K, Tycko B, Tsukada T, Kanai Y, Sumi S, Namiki H, Taya Y, Shibata T, Nakagama H., Free PMC Article

    10/4/2014
    findings indicate somatic mutation of PHLDA3 is rare in common cancer types; PHLDA3 expression was lost in 22% of prostate cancers; these results indicate that PHLDA3 are altered in prostate cancers by loss of expression

    Expressional and mutational analysis of PHLDA3 gene in common human cancers.
    Yoo NJ, Kim YR, Lee SH.

    12/24/2011
    Study identifies PHLDA3 as a p53 target gene that encodes a PH domain-only protein and finds that PHLDA3 competes with the PH domain of Akt for binding of membrane lipids, inhibiting Akt translocation to the cellular membrane and activation.

    PH domain-only protein PHLDA3 is a p53-regulated repressor of Akt.
    Kawase T, Ohki R, Shibata T, Tsutsumi S, Kamimura N, Inazawa J, Ohta T, Ichikawa H, Aburatani H, Tashiro F, Taya Y.

    01/21/2010
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