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    SLC27A5 solute carrier family 27 member 5 [ Homo sapiens (human) ]

    Gene ID: 10998, updated on 11-Apr-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Metabolic Enzyme SLC27A5 Regulates PIP4K2A pre-mRNA Splicing as a Noncanonical Mechanism to Suppress Hepatocellular Carcinoma Metastasis.

    Metabolic Enzyme SLC27A5 Regulates PIP4K2A pre-mRNA Splicing as a Noncanonical Mechanism to Suppress Hepatocellular Carcinoma Metastasis.
    Nie D, Tang X, Deng H, Yang X, Tao J, Xu F, Liu Y, Wu K, Wang K, Mei Z, Huang A, Tang N., Free PMC Article

    02/7/2024
    Copper metabolism-related risk score identifies hepatocellular carcinoma subtypes and SLC27A5 as a potential regulator of cuproptosis.

    Copper metabolism-related risk score identifies hepatocellular carcinoma subtypes and SLC27A5 as a potential regulator of cuproptosis.
    Li X, Wang J, Guo Z, Ma Y, Xu D, Fan D, Dai P, Chen Y, Liu Q, Jiao J, Fan J, Wu N, Li X, Li G., Free PMC Article

    01/29/2024
    Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.

    Loss of SLC27A5 Activates Hepatic Stellate Cells and Promotes Liver Fibrosis via Unconjugated Cholic Acid.
    Wu K, Liu Y, Xia J, Liu J, Wang K, Liang H, Xu F, Liu D, Nie D, Tang X, Huang A, Chen C, Tang N., Free PMC Article

    01/27/2024
    SLC27A5 promotes sorafenib-induced ferroptosis in hepatocellular carcinoma by downregulating glutathione reductase.

    SLC27A5 promotes sorafenib-induced ferroptosis in hepatocellular carcinoma by downregulating glutathione reductase.
    Xu FL, Wu XH, Chen C, Wang K, Huang LY, Xia J, Liu Y, Shan XF, Tang N., Free PMC Article

    01/21/2023
    SLC27A5 deficiency activates NRF2/TXNRD1 pathway by increased lipid peroxidation in HCC.

    SLC27A5 deficiency activates NRF2/TXNRD1 pathway by increased lipid peroxidation in HCC.
    Gao Q, Zhang G, Zheng Y, Yang Y, Chen C, Xia J, Liang L, Lei C, Hu Y, Cai X, Zhang W, Tang H, Chen Y, Huang A, Wang K, Tang N., Free PMC Article

    07/3/2021
    Hepatic FATP5 expression is associated with histological progression and loss of hepatic fat in NAFLD patients.

    Hepatic FATP5 expression is associated with histological progression and loss of hepatic fat in NAFLD patients.
    Enooku K, Tsutsumi T, Kondo M, Fujiwara N, Sasako T, Shibahara J, Kado A, Okushin K, Fujinaga H, Nakagomi R, Minami T, Sato M, Uchino K, Nakagawa H, Kondo Y, Asaoka Y, Tateishi R, Ueki K, Ikeda H, Yoshida H, Moriya K, Yotsuyanagi H, Kadowaki T, Koike K.

    06/5/2021
    Based on a study of 10 pediatric patients, genetic defects that disrupt bile acid amidation cause fat-soluble vitamin deficiency and growth failure, indicating the importance of bile acid conjugation in lipid absorption.

    Genetic defects in bile acid conjugation cause fat-soluble vitamin deficiency.
    Setchell KD, Heubi JE, Shah S, Lavine JE, Suskind D, Al-Edreesi M, Potter C, Russell DW, O'Connell NC, Wolfe B, Jha P, Zhang W, Bove KE, Knisely AS, Hofmann AF, Rosenthal P, Bull LN., Free PMC Article

    06/15/2013
    Bile acid-CoA ligase deficiency is a new inborn error of bile acid metabolism [case report]

    Bile acid-CoA ligase deficiency--a new inborn error of bile acid metabolism.
    Chong CP, Mills PB, McClean P, Gissen P, Bruce C, Stahlschmidt J, Knisely AS, Clayton PT.

    08/11/2012
    A promoter polymorphism in the FATP5 is associated with the metabolic syndrome and steatosis.

    A promoter polymorphism in the liver-specific fatty acid transport protein 5 is associated with features of the metabolic syndrome and steatosis.
    Auinger A, Valenti L, Pfeuffer M, Helwig U, Herrmann J, Fracanzani AL, Dongiovanni P, Fargion S, Schrezenmeir J, Rubin D, Auinger A, Valenti L, Pfeuffer M, Helwig U, Herrmann J, Fracanzani AL, Dongiovanni P, Fargion S, Schrezenmeir J, Rubin D.

    03/5/2011
    Observational study of gene-disease association. (HuGE Navigator)See all PubMed (2) articles

    A promoter polymorphism in the liver-specific fatty acid transport protein 5 is associated with features of the metabolic syndrome and steatosis.
    Auinger A, Valenti L, Pfeuffer M, Helwig U, Herrmann J, Fracanzani AL, Dongiovanni P, Fargion S, Schrezenmeir J, Rubin D, Auinger A, Valenti L, Pfeuffer M, Helwig U, Herrmann J, Fracanzani AL, Dongiovanni P, Fargion S, Schrezenmeir J, Rubin D.

    Candidate gene association study of type 2 diabetes in a nested case-control study of the EPIC-Potsdam cohort - role of fat assimilation.
    Fisher E, Nitz I, Lindner I, Rubin D, Boeing H, Möhlig M, Hampe J, Schreiber S, Schrezenmeir J, Döring F.

    03/13/2008
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