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    PRODH proline dehydrogenase 1 [ Homo sapiens (human) ]

    Gene ID: 5625, updated on 2-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Proline Dehydrogenase (PRODH) Is Expressed in Lung Adenocarcinoma and Modulates Cell Survival and 3D Growth by Inducing Cellular Senescence.

    Proline Dehydrogenase (PRODH) Is Expressed in Lung Adenocarcinoma and Modulates Cell Survival and 3D Growth by Inducing Cellular Senescence.
    Grossi S, Berno E, Chiofalo P, Chiaravalli AM, Cinquetti R, Bruno A, Palano MT, Gallazzi M, La Rosa S, Sessa F, Acquati F, Campomenosi P., Free PMC Article

    01/31/2024
    Prognostic and immunomodulatory roles of schizophrenia-associated genes HTR2A, COMT, and PRODH in pan-cancer analysis and glioma survival prediction model.

    Prognostic and immunomodulatory roles of schizophrenia-associated genes HTR2A, COMT, and PRODH in pan-cancer analysis and glioma survival prediction model.
    Shen J, Wang Q, Lu F, Xu H, Wang P, Feng Y., Free PMC Article

    08/16/2023
    Impact of COMT, PRODH and DISC1 Genetic Variants on Cognitive Performance of Patients with Schizophrenia.

    Impact of COMT, PRODH and DISC1 Genetic Variants on Cognitive Performance of Patients with Schizophrenia.
    Fricke-Galindo I, Pérez-Aldana BE, Macías-Kauffer LR, González-Arredondo S, Dávila-Ortiz de Montellano D, Aviña-Cervantes CL, López-López M, Rodríguez-Agudelo Y, Monroy-Jaramillo N.

    06/11/2022
    Metformin Treatment or PRODH/POX-Knock out Similarly Induces Apoptosis by Reprograming of Amino Acid Metabolism, TCA, Urea Cycle and Pentose Phosphate Pathway in MCF-7 Breast Cancer Cells.

    Metformin Treatment or PRODH/POX-Knock out Similarly Induces Apoptosis by Reprograming of Amino Acid Metabolism, TCA, Urea Cycle and Pentose Phosphate Pathway in MCF-7 Breast Cancer Cells.
    Huynh TYL, Oscilowska I, Sáiz J, Nizioł M, Baszanowska W, Barbas C, Palka J., Free PMC Article

    01/22/2022
    Understanding the role of key amino acids in regulation of proline dehydrogenase/proline oxidase (prodh/pox)-dependent apoptosis/autophagy as an approach to targeted cancer therapy.

    Understanding the role of key amino acids in regulation of proline dehydrogenase/proline oxidase (prodh/pox)-dependent apoptosis/autophagy as an approach to targeted cancer therapy.
    Huynh TYL, Zareba I, Baszanowska W, Lewoniewska S, Palka J., Free PMC Article

    10/10/2020
    Proline Dehydrogenase (PRODH) expression is reduced in human with Heart Failure. PRODH appears to be crucial to sustain normal mitochondrial function and maintenance of ATP levels in human cardiomyocytes in a hypoxic environment, as well as for redox homeostasis in both normoxic and hypoxic conditions.

    Exercise Reveals Proline Dehydrogenase as a Potential Target in Heart Failure.
    Moreira JBN, Wohlwend M, Fenk S, Åmellem I, Flatberg A, Kraljevic J, Marinovic J, Ljubkovic M, Bjørkøy G, Wisløff U.

    04/20/2019
    PRODH1-mediated proline metabolism promotes pancreatic ductal adenocarcinoma growth.

    Collagen-derived proline promotes pancreatic ductal adenocarcinoma cell survival under nutrient limited conditions.
    Olivares O, Mayers JR, Gouirand V, Torrence ME, Gicquel T, Borge L, Lac S, Roques J, Lavaut MN, Berthezène P, Rubis M, Secq V, Garcia S, Moutardier V, Lombardo D, Iovanna JL, Tomasini R, Guillaumond F, Vander Heiden MG, Vasseur S., Free PMC Article

    12/22/2018
    Here, we show that Prodh-deficient mice with elevated CNS L-proline display specific deficits in high-frequency GABA-ergic transmission and gamma-band oscillations. We find that L-proline is a GABA-mimetic and can act at multiple GABA-ergic targets

    Cytosolic Accumulation of L-Proline Disrupts GABA-Ergic Transmission through GAD Blockade.
    Crabtree GW, Park AJ, Gordon JA, Gogos JA., Free PMC Article

    12/2/2017
    PRODH/POX knockdown decreased DNA and collagen biosynthesis, whereas increased prolidase activity and intracellular proline level in MCF-7shPRODH/POX cells.

    Functional Consequences of Intracellular Proline Levels Manipulation Affecting PRODH/POX-Dependent Pro-Apoptotic Pathways in a Novel in Vitro Cell Culture Model.
    Zareba I, Surazynski A, Chrusciel M, Miltyk W, Doroszko M, Rahman N, Palka J.

    11/4/2017
    this study shows that PRODH plays a causative role in DNA damage-induced senescence through the enzymatic generation of reactive oxygen species

    Proline dehydrogenase promotes senescence through the generation of reactive oxygen species.
    Nagano T, Nakashima A, Onishi K, Kawai K, Awai Y, Kinugasa M, Iwasaki T, Kikkawa U, Kamada S.

    05/6/2017
    the frequency of a recurrent small 22q11.2 deletion encompassing PRODH and the neighboring DGCR6 gene in three case-control studies, was studied.

    The 22q11 PRODH/DGCR6 deletion is frequent in hyperprolinemic subjects but is not a strong risk factor for ASD.
    Richard AC, Rovelet-Lecrux A, Delaby E, Charbonnier C, Thiruvahindrapuram B, Hatchwell E, Eis PS, Afenjar A, Gilbert Dussardier B, Scherer SW, Betancur C, Campion D.

    12/17/2016
    The findings support a major role for the PRODH 757TT, 1766GG, and 1852AA genotypes alone and in combination for schizophrenia susceptibility.

    Relationship between polymorphisms in the proline dehydrogenase gene and schizophrenia risk.
    Ghasemvand F, Omidinia E, Salehi Z, Rahmanzadeh S.

    07/30/2016
    Thirty-five percent of the subjects were hyperprolinemic, allele carriers of PRODH rs450046 had a lower full-scale intelligence compared to T allele carriers

    PRODH rs450046 and proline x COMT Val¹⁵⁸ Met interaction effects on intelligence and startle in adults with 22q11 deletion syndrome.
    de Koning MB, van Duin ED, Boot E, Bloemen OJ, Bakker JA, Abel KM, van Amelsvoort TA.

    03/12/2016
    GR and KLF15 physically interact via low affinity GR binding sites within glucocorticoid response elements (GREs) for PRODH and AASS that contribute to combinatorial regulation with KLF15.

    Response Element Composition Governs Correlations between Binding Site Affinity and Transcription in Glucocorticoid Receptor Feed-forward Loops.
    Sasse SK, Zuo Z, Kadiyala V, Zhang L, Pufall MA, Jain MK, Phang TL, Stormo GD, Gerber AN., Free PMC Article

    11/7/2015
    results suggest that PRODH and COMT may interact to contribute to the ASD phenotype in individuals with VCFS

    Association between autism spectrum disorder in individuals with velocardiofacial (22q11.2 deletion) syndrome and PRODH and COMT genotypes.
    Radoeva PD, Coman IL, Salazar CA, Gentile KL, Higgins AM, Middleton FA, Antshel KM, Fremont W, Shprintzen RJ, Morrow BE, Kates WR., Free PMC Article

    06/27/2015
    Functional COMT, but not PRODH, variant affects IQ and executive functions in 22q11.2DS subjects during neurodevelopment with a maximal effect at adulthood

    Association of COMT and PRODH gene variants with intelligence quotient (IQ) and executive functions in 22q11.2DS subjects.
    Carmel M, Zarchi O, Michaelovsky E, Frisch A, Patya M, Green T, Gothelf D, Weizman A.

    02/21/2015
    Data indicate that a functional proline dehydrogenase (PRODH) variant associated with schizophrenia that may have a neurochemical impact, altering brain function, but is not responsible for the cortical reductions found in the disorder.

    PRODH polymorphisms, cortical volumes and thickness in schizophrenia.
    Ota VK, Bellucco FT, Gadelha A, Santoro ML, Noto C, Christofolini DM, Assunção IB, Yamada KM, Ribeiro-dos-Santos AK, Santos S, Mari JJ, Smith MA, Melaragno MI, Bressan RA, Sato JR, Jackowski AP, Belangero SI., Free PMC Article

    12/6/2014
    The current study demonstrates that sensory gating impairments that are typical of schizophrenia are found in 22q11.2DS subjects. Our results further suggest that COMT and PRODH genetic variations contribute to sensory gating.

    Schizophrenia-like neurophysiological abnormalities in 22q11.2 deletion syndrome and their association to COMT and PRODH genotypes.
    Zarchi O, Carmel M, Avni C, Attias J, Frisch A, Michaelovsky E, Patya M, Green T, Weinberger R, Weizman A, Gothelf D.

    05/17/2014
    PRODH, but not PRODH2, expression is under the control of p53 family members, specifically p53 and p73.

    P53 family members modulate the expression of PRODH, but not PRODH2, via intronic p53 response elements.
    Raimondi I, Ciribilli Y, Monti P, Bisio A, Pollegioni L, Fronza G, Inga A, Campomenosi P., Free PMC Article

    02/15/2014
    Human-specific endogenous retroviral insert serves as an enhancer for the schizophrenia-linked gene PRODH.

    Human-specific endogenous retroviral insert serves as an enhancer for the schizophrenia-linked gene PRODH.
    Suntsova M, Gogvadze EV, Salozhin S, Gaifullin N, Eroshkin F, Dmitriev SE, Martynova N, Kulikov K, Malakhova G, Tukhbatova G, Bolshakov AP, Ghilarov D, Garazha A, Aliper A, Cantor CR, Solokhin Y, Roumiantsev S, Balaban P, Zhavoronkov A, Buzdin A., Free PMC Article

    02/1/2014
    distinct molecular alterations of the PRODH gene result in abnormal proline levels.

    Identification of PRODH mutations in Korean neonates with type I hyperprolinemia.
    Jang MA, Kim BC, Ki CS, Lee SY, Kim JW, Choi TY, Lee DH, Song J, Lee YW, Park HD.

    08/31/2013
    results provide evidence that PRODH is essential in proline protection against hydrogen peroxide-mediated cell death and that proline/PRODH helps activate Akt in cancer cells

    Proline dehydrogenase is essential for proline protection against hydrogen peroxide-induced cell death.
    Natarajan SK, Zhu W, Liang X, Zhang L, Demers AJ, Zimmerman MC, Simpson MA, Becker DF., Free PMC Article

    06/8/2013
    There is no association between proline dehydrogenase (oxidase) 1 polymorphisms and schizophrenia in Korean population

    Lack of association between proline dehydrogenase (oxidase) 1 polymorphisms and schizophrenia in a Korean population.
    Kim JH, Park BL, Pasaje CF, Bae JS, Park CS, Cha B, Kim BJ, Kim JW, Choi WH, Shin TM, Choi IG, Hwang J, Woo SI, Shin HD.

    10/6/2012
    The findings from this study showed that troglitazone-induced apoptosis was mediated by POX-induced ROS formation, at least partly, via PPARgamma activation.

    Troglitazone induced apoptosis via PPARγ activated POX-induced ROS formation in HT29 cells.
    Wang J, Lv X, Shi J, Hu X, DU Y.

    01/28/2012
    For a number of genes affected by de novo copy number variants CNVs in autism (CNTNAP2, ZNF214, ARID1B, Proline Dehydrogenase), reduced transcript expression may be a mechanism of pathogenesis during neurodevelopment.

    Reduced transcript expression of genes affected by inherited and de novo CNVs in autism.
    Nord AS, Roeb W, Dickel DE, Walsh T, Kusenda M, O'Connor KL, Malhotra D, McCarthy SE, Stray SM, Taylor SM, Sebat J, STAART Psychopharmacology Network, King B, King MC, McClellan JM., Free PMC Article

    09/17/2011
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