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    ATP5F1A ATP synthase F1 subunit alpha [ Homo sapiens (human) ]

    Gene ID: 498, updated on 6-Oct-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling.

    Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling.
    Xu M, Zhang H, Chang Y, Hua X, Chen X, Sheng Y, Shan D, Bao M, Hu S, Song J., Free PMC Article

    08/14/2024
    BRG1 promotes liver cancer cell proliferation and metastasis by enhancing mitochondrial function and ATP5A1 synthesis through TOMM40.

    BRG1 promotes liver cancer cell proliferation and metastasis by enhancing mitochondrial function and ATP5A1 synthesis through TOMM40.
    Hui Y, Leng J, Jin D, Wang G, Liu K, Bu Y, Wang Q., Free PMC Article

    07/26/2024
    Proteomic analyses identify HK1 and ATP5A to be overexpressed in distant metastases of lung adenocarcinomas compared to matched primary tumors.

    Proteomic analyses identify HK1 and ATP5A to be overexpressed in distant metastases of lung adenocarcinomas compared to matched primary tumors.
    Pasternack H, Polzer M, Gemoll T, Kümpers C, Sauer T, Lazar-Karsten P, Hinrichs S, Bohnet S, Perner S, Dressler FF, Kirfel J., Free PMC Article

    12/1/2023
    Meta-analysis of brain samples of individuals with schizophrenia detects down-regulation of multiple ATP synthase encoding genes in both females and males.

    Meta-analysis of brain samples of individuals with schizophrenia detects down-regulation of multiple ATP synthase encoding genes in both females and males.
    Katz Shroitman N, Yitzhaky A, Ben Shachar D, Gurwitz D, Hertzberg L.

    02/11/2023
    Growth arrest and DNA damage-inducible alpha regulates muscle repair and fat infiltration through ATP synthase F1 subunit alpha.

    Growth arrest and DNA damage-inducible alpha regulates muscle repair and fat infiltration through ATP synthase F1 subunit alpha.
    You W, Liu S, Ji J, Ling D, Tu Y, Zhou Y, Chen W, Valencak TG, Wang Y, Shan T., Free PMC Article

    02/11/2023
    A recurrent de novo ATP5F1A substitution associated with neonatal complex V deficiency.

    A recurrent de novo ATP5F1A substitution associated with neonatal complex V deficiency.
    Lines MA, Cuillerier A, Chakraborty P, Naas T, Duque Lasio ML, Michaud J, Pileggi C, Harper ME, Burelle Y, Toler TL, Sondheimer N, Crawford HP, Millan F, Geraghty MT., Free PMC Article

    03/26/2022
    ATP5A1 Participates in Transcriptional and Posttranscriptional Regulation of Cancer-Associated Genes by Modulating Their Expression and Alternative Splicing Profiles in HeLa Cells.

    ATP5A1 Participates in Transcriptional and Posttranscriptional Regulation of Cancer-Associated Genes by Modulating Their Expression and Alternative Splicing Profiles in HeLa Cells.
    Song Ba Y, Wang Ma F, Wei Ma Y, Chen Ba D, Deng Ba G., Free PMC Article

    01/29/2022
    Defining the molecular mechanisms of the mitochondrial permeability transition through genetic manipulation of F-ATP synthase.

    Defining the molecular mechanisms of the mitochondrial permeability transition through genetic manipulation of F-ATP synthase.
    Carrer A, Tommasin L, Šileikytė J, Ciscato F, Filadi R, Urbani A, Forte M, Rasola A, Szabò I, Carraro M, Bernardi P., Free PMC Article

    08/28/2021
    F0F1 ATP synthase regulates extracellular calcium influx in human neutrophils by interacting with Cav2.3 and modulates neutrophil accumulation in the lipopolysaccharide-challenged lung.

    F0F1 ATP synthase regulates extracellular calcium influx in human neutrophils by interacting with Ca(v)2.3 and modulates neutrophil accumulation in the lipopolysaccharide-challenged lung.
    Zhu B, Feng Z, Guo Y, Zhang T, Mai A, Kang Z, Weijen T, Wang D, Yin D, Zhu D, Gao J., Free PMC Article

    06/12/2021
    Poly(GR) bound preferentially to the mitochondrial complex V component ATP5A1 and enhanced its ubiquitination and degradation, consistent with reduced ATP5A1 protein level in both (GR)80 mouse neurons and amyotrophic lateral sclerosis and frontotemporal dementia patient brains

    C9ORF72-ALS/FTD-associated poly(GR) binds Atp5a1 and compromises mitochondrial function in vivo.
    Choi SY, Lopez-Gonzalez R, Krishnan G, Phillips HL, Li AN, Seeley WW, Yao WD, Almeida S, Gao FB., Free PMC Article

    07/6/2019
    The study demonstrates a novel role of FANCD2 in governing cellular ATP production via ATP5A, and advances the understanding of how defective Fanconi anemia signaling contributes to aging and cancer at the energy metabolism level.

    Involvement of FANCD2 in Energy Metabolism via ATP5α.
    Jayabal P, Ma C, Nepal M, Shen Y, Che R, Turkson J, Fei P., Free PMC Article

    01/12/2019
    17% of prostate carcinomas and 18% of benign prostate tissues showed isolated or combined deficiency of oxidative phosphorylation complexes. ATP5F1A, a complex V protein, was the most frequently affected subunit

    Reduced Levels of ATP Synthase Subunit ATP5F1A Correlate with Earlier-Onset Prostate Cancer.
    Feichtinger RG, Schäfer G, Seifarth C, Mayr JA, Kofler B, Klocker H., Free PMC Article

    01/12/2019
    Using systems biology techniques to study gene coexpression network, ATP5A1 was identified and found highly expressed in normal kidney than clear cell renal cell carcinoma (ccRCC) tissues of each grade. Functional and pathway enrichment analysis demonstrated that ATP5A1 is overrepresented in pathway of oxidative phosphorylation, which associated with tumorigenesis and tumor progression.

    A novel correlation between ATP5A1 gene expression and progression of human clear cell renal cell carcinoma identified by co‑expression analysis.
    Yuan L, Chen L, Qian K, Wang G, Lu M, Qian G, Cao X, Jiang W, Xiao Y, Wang X., Free PMC Article

    09/8/2018
    This cohort study showed that the ATP5A1 gene was down regulation between patients with idiopathic Parkinson disease and controls

    Analysis of blood-based gene expression in idiopathic Parkinson disease.
    Shamir R, Klein C, Amar D, Vollstedt EJ, Bonin M, Usenovic M, Wong YC, Maver A, Poths S, Safer H, Corvol JC, Lesage S, Lavi O, Deuschl G, Kuhlenbaeumer G, Pawlack H, Ulitsky I, Kasten M, Riess O, Brice A, Peterlin B, Krainc D., Free PMC Article

    10/28/2017
    these data highlight a key role of the P2Y1/PI3Kbeta axis in endothelial cell proliferation downstream of ecto-F1-ATPase activation by apoA-I. Pharmacological targeting of this pathway could represent a promising approach to enhance vascular endothelial protection.

    PI3Kβ Plays a Key Role in Apolipoprotein A-I-Induced Endothelial Cell Proliferation Through Activation of the Ecto-F1-ATPase/P2Y1 Receptors.
    Castaing-Berthou A, Malet N, Radojkovic C, Cabou C, Gayral S, Martinez LO, Laffargue M.

    08/5/2017
    These findings, together with the previously reported inhibition of respiratory complex I, show that depression of the activity of oxidative phosphorylation enzymes is involved in the cell growth inhibitory action of ATRA.

    All trans retinoic acid depresses the content and activity of the mitochondrial ATP synthase in human keratinocytes.
    Papa F, Lippolis R, Sardaro N, Gnoni A, Scacco S.

    05/27/2017
    High mRNA levels of ATP5A1 are associated with glioblastoma.

    ATP5A1 and ATP5B are highly expressed in glioblastoma tumor cells and endothelial cells of microvascular proliferation.
    Xu G, Li JY.

    11/5/2016
    Hemoglobin - a novel ligand of hepatocyte ectopic F1-ATPase

    Hemoglobin - a novel ligand of hepatocyte ectopic F1-ATPase.
    Gburek J, Konopska B, Juszczynska K, Piwowar A, Dziegiel P, Borska S, Tolosano E, Golab K.

    10/29/2016
    Here, we found that ATP synthase subunit alpha (ATP5A) was O-GlcNAcylated at Thr432 and ATP5A O-GlcNAcylation was decreased in the brains of AD patients and transgenic mouse model

    Mitochondrial ATP synthase activity is impaired by suppressed O-GlcNAcylation in Alzheimer's disease.
    Cha MY, Cho HJ, Kim C, Jung YO, Kang MJ, Murray ME, Hong HS, Choi YJ, Choi H, Kim DK, Choi H, Kim J, Dickson DW, Song HK, Cho JW, Yi EC, Kim J, Jin SM, Mook-Jung I., Free PMC Article

    09/17/2016
    Mitochondrial calpain-1 disrupts ATP synthase, leading to mitochondrial reactive oxygen species generation, which promotes proinflammatory response and myocardial dysfunction during endotoxemia.

    Deletion of capn4 Protects the Heart Against Endotoxemic Injury by Preventing ATP Synthase Disruption and Inhibiting Mitochondrial Superoxide Generation.
    Ni R, Zheng D, Wang Q, Yu Y, Chen R, Sun T, Wang W, Fan GC, Greer PA, Gardiner RB, Peng T., Free PMC Article

    12/5/2015
    Studies indicate that the F-ATP synthase can reversibly undergo a Ca(2+)-dependent transition to form a channel that mediates the permeability transition.

    From ATP to PTP and Back: A Dual Function for the Mitochondrial ATP Synthase.
    Bernardi P, Di Lisa F, Fogolari F, Lippe G., Free PMC Article

    08/8/2015
    A mutation in ATP5A1 causes a fatal neonatal mitochondrial encephalopathy.

    A complex V ATP5A1 defect causes fatal neonatal mitochondrial encephalopathy.
    Jonckheere AI, Renkema GH, Bras M, van den Heuvel LP, Hoischen A, Gilissen C, Nabuurs SB, Huynen MA, de Vries MC, Smeitink JA, Rodenburg RJ.

    06/29/2013
    Studies indicate that F1-ATPase (F1) is a rotary motor protein driven by ATP hydrolysis and the minimum complex of F1 for function as a rotary motor is the alpha3beta3gamma subcomplex.

    Chemomechanical coupling mechanism of F(1)-ATPase: catalysis and torque generation.
    Watanabe R, Noji H.

    06/1/2013
    Homozygous mutations in this gene are the likely cause of mitochondrial disease in two sisters, with support from a yeast model.

    Targeted exome sequencing of suspected mitochondrial disorders.
    Lieber DS, Calvo SE, Shanahan K, Slate NG, Liu S, Hershman SG, Gold NB, Chapman BA, Thorburn DR, Berry GT, Schmahmann JD, Borowsky ML, Mueller DM, Sims KB, Mootha VK., Free PMC Article

    04/25/2013
    F1-ATPase at the cell surface of colonic epithelial cells has a role in mediating cell proliferation

    Identification of the F1-ATPase at the cell surface of colonic epithelial cells: role in mediating cell proliferation.
    Kowalski-Chauvel A, Najib S, Tikhonova IG, Huc L, Lopez F, Martinez LO, Cohen-Jonathan-Moyal E, Ferrand A, Seva C., Free PMC Article

    02/9/2013
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