U.S. flag

An official website of the United States government

Format

Send to:

Choose Destination
    • Showing Current items.

    AATF apoptosis antagonizing transcription factor [ Homo sapiens (human) ]

    Gene ID: 26574, updated on 4-Jan-2025

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Vinblastine Resistance Is Associated with Nephronophthisis 3-Mediated Primary Cilia via Intraflagellar Transport Protein 88 and Apoptosis-Antagonizing Transcription Factor.

    Vinblastine Resistance Is Associated with Nephronophthisis 3-Mediated Primary Cilia via Intraflagellar Transport Protein 88 and Apoptosis-Antagonizing Transcription Factor.
    Thuy PX, Jang TK, Moon EY., Free PMC Article

    10/22/2024
    HAX1 is a novel binding partner of Che-1/AATF. Implications in oxidative stress cell response.

    HAX1 is a novel binding partner of Che-1/AATF. Implications in oxidative stress cell response.
    Pisani C, Onori A, Gabanella F, Iezzi S, De Angelis R, Fanciulli M, Colizza A, de Vincentiis M, Di Certo MG, Passananti C, Corbi N.

    11/20/2023
    CK2-mediated phosphorylation of Che-1/AATF is required for its pro-proliferative activity.

    CK2-mediated phosphorylation of Che-1/AATF is required for its pro-proliferative activity.
    Catena V, Bruno T, Iezzi S, Matteoni S, Salis A, Sorino C, Damonte G, Fanciulli M., Free PMC Article

    12/25/2021
    AATF and SMARCA2 are associated with thyroid volume in Hashimoto's thyroiditis patients.

    AATF and SMARCA2 are associated with thyroid volume in Hashimoto's thyroiditis patients.
    Brčić L, Barić A, Benzon B, Brekalo M, Gračan S, Kaličanin D, Škrabić V, Zemunik T, Barbalić M, Novak I, Pešutić Pisac V, Punda A, Boraska Perica V., Free PMC Article

    11/21/2020
    Che-1/AATF binds to RNA polymerase I machinery and sustains ribosomal RNA gene transcription.

    Che-1/AATF binds to RNA polymerase I machinery and sustains ribosomal RNA gene transcription.
    Sorino C, Catena V, Bruno T, De Nicola F, Scalera S, Bossi G, Fabretti F, Mano M, De Smaele E, Fanciulli M, Iezzi S., Free PMC Article

    09/12/2020
    drives hepatocarcinogenesis in nonalcoholic fatty liver disease

    A Regulatory Role of Apoptosis Antagonizing Transcription Factor in the Pathogenesis of Nonalcoholic Fatty Liver Disease and Hepatocellular Carcinoma.
    Kumar DP, Santhekadur PK, Seneshaw M, Mirshahi F, Uram-Tuculescu C, Sanyal AJ., Free PMC Article

    05/30/2020
    miR-663 may function as an 'apoptomiR' by inhibiting the anti-apoptotic gene AATF to induce apoptosis. These findings could have therapeutic implications for epithelial cell targeting in cancer therapy.

    MicroRNA-663 antagonizes apoptosis antagonizing transcription factor to induce apoptosis in epithelial cells.
    Benakanakere MR, Zhao J, Finoti L, Schattner R, Odabas-Yigit M, Kinane DF.

    04/25/2020
    These data individuate Che-1 as a possible novel target in the treatment of B-cell precursor acute lymphoblastic leukemia able to affect c-Myc-driven tumorigenicity.

    A new baby in the c-Myc-directed transcriptional machinery: Che-1/AATF.
    Folgiero V, Sorino C, Locatelli F, Fanciulli M., Free PMC Article

    11/2/2019
    Identification of the transcriptional regulator AATF/CHE-1 as a key molecule to sustain proliferative tissues and tumor progression in parts by inhibiting p53-driven apoptosis in vivo.

    AATF suppresses apoptosis, promotes proliferation and is critical for Kras-driven lung cancer.
    Welcker D, Jain M, Khurshid S, Jokić M, Höhne M, Schmitt A, Frommolt P, Niessen CM, Spiro J, Persigehl T, Wittersheim M, Büttner R, Fanciulli M, Schermer B, Reinhardt HC, Benzing T, Höpker K.

    03/23/2019
    Genomewide ChIP-seq experiments suggest that Che-1 acts as a downstream effector of c-Myc. These results identify the pivotal role of Che-1 in the control of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) proliferation and present the protein as a possible therapeutic target in children with relapsed BCP-ALL

    Che-1 is targeted by c-Myc to sustain proliferation in pre-B-cell acute lymphoblastic leukemia.
    Folgiero V, Sorino C, Pallocca M, De Nicola F, Goeman F, Bertaina V, Strocchio L, Romania P, Pitisci A, Iezzi S, Catena V, Bruno T, Strimpakos G, Passananti C, Mattei E, Blandino G, Locatelli F, Fanciulli M., Free PMC Article

    02/9/2019
    Results show that Che-1 protects colon cancer cells from apoptosis induced by hypoxia through its ability to regulate HIF1-alpha stabilization in colorectal cancer cells.

    Che-1 sustains hypoxic response of colorectal cancer cells by affecting Hif-1α stabilization.
    Bruno T, Valerio M, Casadei L, De Nicola F, Goeman F, Pallocca M, Catena V, Iezzi S, Sorino C, Desantis A, Manetti C, Blandino G, Floridi A, Fanciulli M., Free PMC Article

    12/16/2017
    Results show that eEF1Bgamma binds to the Che-1 promoter region and its transcript, and describe a novel mitochondrial localization for the Che-1 protein which needs mitochondrial integrity for correct localization.

    eEF1Bγ binds the Che-1 and TP53 gene promoters and their transcripts.
    Pisani C, Onori A, Gabanella F, Delle Monache F, Borreca A, Ammassari-Teule M, Fanciulli M, Di Certo MG, Passananti C, Corbi N., Free PMC Article

    12/16/2017
    we identified the ANN complex as a novel functional module supporting the nucleolar maturation of 40S ribosomal subunits. Our data help to explain the described role of AATF in cell proliferation during mouse development as well as its requirement for malignant tumor growth.

    Human AATF/Che-1 forms a nucleolar protein complex with NGDN and NOL10 required for 40S ribosomal subunit synthesis.
    Bammert L, Jonas S, Ungricht R, Kutay U., Free PMC Article

    06/10/2017
    the effect of APOBEC3G over-expression upon AATF gene expression, was examined.

    APOBEC3G governs the generation of truncated AATF protein to ensure oncogenic transformation.
    Sharma S, Garg A, Dhanda RS, Kaul D.

    02/4/2017
    loss of Che-1 inhibits proliferation and promotes apoptosis in MG-63 cells by decreasing the level of mutant p53

    Che-1 gene silencing induces osteosarcoma cell apoptosis by inhibiting mutant p53 expression.
    Liu M, Wang D, Li N.

    09/24/2016
    It was concluded that PARP-1 was involved in the DNA damage repair induced by HQ via increasing the accumulation of apoptosis antagonizing transcription factor through PARylation.

    Poly(ADP-ribosyl)ation of Apoptosis Antagonizing Transcription Factor Involved in Hydroquinone-Induced DNA Damage Response.
    Ling XX, Liu JX, Yun L, DU YJ, Chen SQ, Chen JL, Tang HW, Liu LH.

    05/21/2016
    These results confirm Che-1 as an important regulator of p53 activity and suggest Che-1 to be a promising yet attractive drug target for cancer therapy.

    Che-1 modulates the decision between cell cycle arrest and apoptosis by its binding to p53.
    Desantis A, Bruno T, Catena V, De Nicola F, Goeman F, Iezzi S, Sorino C, Gentileschi MP, Germoni S, Monteleone V, Pellegrino M, Kann M, De Meo PD, Pallocca M, Höpker K, Moretti F, Mattei E, Reinhardt HC, Floridi A, Passananti C, Benzing T, Blandino G, Fanciulli M., Free PMC Article

    02/20/2016
    In the face of high glucose threat, mitochondrial UCP2 gene expression is regulated by miR-2909 and AATF.

    Mitochondrial uncoupling protein (UCP2) gene expression is regulated by miR-2909.
    Kaul D, Sharma S, Garg A.

    02/6/2016
    This mutant AATF along with its interactome consisting of SP1, DNMT3B and Par-4 ensures cancer cell DNA methylation required for down-regulation of tumor suppressor genes.

    Oncogenic nature of a novel mutant AATF and its interactome existing within human cancer cells.
    Sharma S, Kaul D, Arora M, Malik D.

    10/24/2015
    HIPK2 depletion strongly decreases Che-1 ubiquitylation and degradation.

    HIPK2 sustains apoptotic response by phosphorylating Che-1/AATF and promoting its degradation.
    De Nicola F, Catena V, Rinaldo C, Bruno T, Iezzi S, Sorino C, Desantis A, Camerini S, Crescenzi M, Floridi A, Passananti C, Soddu S, Fanciulli M., Free PMC Article

    07/25/2015
    Che-1 expression correlates with the progression of multiple myeloma and is required for cell growth and survival.Che-1 controls mTOR through the induction of Redd1 and Deptor, two important repressors of mTOR.

    Che-1-induced inhibition of mTOR pathway enables stress-induced autophagy.
    Desantis A, Bruno T, Catena V, De Nicola F, Goeman F, Iezzi S, Sorino C, Ponzoni M, Bossi G, Federico V, La Rosa F, Ricciardi MR, Lesma E, De Meo PD, Castrignanò T, Petrucci MT, Pisani F, Chesi M, Bergsagel PL, Floridi A, Tonon G, Passananti C, Blandino G, Fanciulli M., Free PMC Article

    07/25/2015
    Cell proliferation decreased by 41% which was accompanied by apoptosis induction in 30% MCF-7 cells after AATF gene knockdown.

    Apoptosis-antagonizing transcription factor (AATF) gene silencing: role in induction of apoptosis and down-regulation of estrogen receptor in breast cancer cells.
    Sharma M.

    04/19/2014
    Che-1 depletion abolishes the ability of Chk1 to bind pericentrin and to localize at centrosomes, which, in its turn, deregulates the activation of centrosomal cyclin B-Cdk1 and advances entry into mitosis.

    Centrosomal Che-1 protein is involved in the regulation of mitosis and DNA damage response by mediating pericentrin (PCNT)-dependent Chk1 protein localization.
    Sorino C, Bruno T, Desantis A, Di Certo MG, Iezzi S, De Nicola F, Catena V, Floridi A, Chessa L, Passananti C, Cundari E, Fanciulli M., Free PMC Article

    11/2/2013
    These results identify AATF as a nucleolar-confined c-Jun cofactor whose expression levels and spatial distribution determine the stress-induced activity of c-Jun and the levels of c-Jun-mediated apoptosis.

    Nucleolar AATF regulates c-Jun-mediated apoptosis.
    Ferraris SE, Isoniemi K, Torvaldson E, Anckar J, Westermarck J, Eriksson JE., Free PMC Article

    04/13/2013
    Nuclear AATF enrichment is selected for in p53-proficient endometrial cancers. Focal copy number AATF gains correlate with reduced overall survival in neuroblastoma. AATF is a critical repressor of p53-driven apoptosis.

    AATF/Che-1 acts as a phosphorylation-dependent molecular modulator to repress p53-driven apoptosis.
    Höpker K, Hagmann H, Khurshid S, Chen S, Hasskamp P, Seeger-Nukpezah T, Schilberg K, Heukamp L, Lamkemeyer T, Sos ML, Thomas RK, Lowery D, Roels F, Fischer M, Liebau MC, Resch U, Kisner T, Röther F, Bartram MP, Müller RU, Fabretti F, Kurschat P, Schumacher B, Gaestel M, Medema RH, Yaffe MB, Schermer B, Reinhardt HC, Benzing T., Free PMC Article

    01/26/2013
    firstprevious page of 2 nextlast