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    ELL elongation factor for RNA polymerase II [ Homo sapiens (human) ]

    Gene ID: 8178, updated on 27-Nov-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Stratification and therapeutic potential of ELL in cytogenetic normal acute myeloid leukemia.

    Stratification and therapeutic potential of ELL in cytogenetic normal acute myeloid leukemia.
    Zha J, Zhong M, Pan G, Chen Q, Jiang Y, Lai Q, Tan J, Zhou H, Wu H, Xu B.

    02/4/2023
    ATM-mediated ELL phosphorylation enhances its self-association through increased EAF1 interaction and inhibits global transcription during genotoxic stress.

    ATM-mediated ELL phosphorylation enhances its self-association through increased EAF1 interaction and inhibits global transcription during genotoxic stress.
    Pal S, Yadav D, Biswas D., Free PMC Article

    11/12/2022
    ELL Facilitates RNA Polymerase II-Mediated Transcription of Human Epidermal Proliferation Genes.

    ELL Facilitates RNA Polymerase II-Mediated Transcription of Human Epidermal Proliferation Genes.
    Li J, Bansal V, Tiwari M, Chen Y, Sen GL., Free PMC Article

    11/22/2021
    E1A-associated p300 protein -mediated site-specific acetylation increases, whereas histone deacetylase 3-mediated deacetylation decreases, transcriptional elongation factor ELL stability through polyubiquitylation by the E3 ubiquitin ligase Siah1. Knockdown of human cell cycle and apoptosis regulator 2 reduces ELL levels and expression of a significant number of genes, including those involved in glucose metabolism.

    DBC1, p300, HDAC3, and Siah1 coordinately regulate ELL stability and function for expression of its target genes.
    Basu S, Barad M, Yadav D, Nandy A, Mukherjee B, Sarkar J, Chakrabarti P, Mukhopadhyay S, Biswas D., Free PMC Article

    08/15/2020
    The results indicate that p53 interferes with the interaction between ELL/EAF and ICE1 and represses transcription of small nuclear RNA genes by Pol II.

    p53 represses the transcription of snRNA genes by preventing the formation of little elongation complex.
    Anwar D, Takahashi H, Watanabe M, Suzuki M, Fukuda S, Hatakeyama S.

    11/4/2017
    This work reveals a previously unrecognized function for ELL as an E3 ubiquitin ligase for c-Myc and a potential tumour suppressor.

    ELL targets c-Myc for proteasomal degradation and suppresses tumour growth.
    Chen Y, Zhou C, Ji W, Mei Z, Hu B, Zhang W, Zhang D, Wang J, Liu X, Ouyang G, Zhou J, Xiao W., Free PMC Article

    09/3/2016
    The Tax oncogene enhances ELL incorporation into p300 and P-TEFb containing protein complexes to activate transcription.

    The Tax oncogene enhances ELL incorporation into p300 and P-TEFb containing protein complexes to activate transcription.
    Fufa TD, Byun JS, Wakano C, Fernandez AG, Pise-Masison CA, Gardner K.

    11/28/2015
    eleven-nineteen lysine-rich leukemia protein enhanced E2F1 deacetylation via recruitment of histone deacetylase 1

    ELL inhibits E2F1 transcriptional activity by enhancing E2F1 deacetylation via recruitment of histone deacetylase 1.
    Zhang W, Ji W, Liu X, Ouyang G, Xiao W., Free PMC Article

    03/22/2014
    ELL is an essential player for RNA Pol II restart during cellular DNA damage response.

    ELL, a novel TFIIH partner, is involved in transcription restart after DNA repair.
    Mourgues S, Gautier V, Lagarou A, Bordier C, Mourcet A, Slingerland J, Kaddoum L, Coin F, Vermeulen W, Gonzales de Peredo A, Monsarrat B, Mari PO, Giglia-Mari G., Free PMC Article

    01/11/2014
    Studies indicate that the super elongation complex (SEC) consisting of ELL, P-TEFb (CDK9) and MLL required for rapid transcriptional induction in the presence or absence of paused RNA polymerase II (Pol II).

    The super elongation complex (SEC) family in transcriptional control.
    Luo Z, Lin C, Shilatifard A.

    11/3/2012
    ELL has an early and essential role during rapid high-amplitude gene expression that is required for both Pol II pause site entry and release

    ELL facilitates RNA polymerase II pause site entry and release.
    Byun JS, Fufa TD, Wakano C, Fernandez A, Haggerty CM, Sung MH, Gardner K., Free PMC Article

    07/28/2012
    Our findings suggest that ELL and HIF-1alpha are binding partners and can modulate the functions of each other in hypoxia.

    ELL is an HIF-1alpha partner that regulates and responds to hypoxia response in PC3 cells.
    Liu L, Ai J, Xiao W, Liu J, Wang Y, Xin D, He Z, Guo Y, Wang Z., Free PMC Article

    05/10/2010
    ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation

    Elongation factor ELL (Eleven-Nineteen Lysine-rich Leukemia) acts as a transcription factor for direct thrombospondin-1 regulation.
    Zhou J, Feng X, Ban B, Liu J, Wang Z, Xiao W., Free PMC Article

    01/21/2010
    In the Acute Myeloid Leukemia patients, detected MLL rearrangements consisting of MLL/AF6, MLL/AF9, MLL/AF17 , MLL/ELL and MLL partial tandem duplication. MLL rearrangement include chromosome translocation and partial tandem duplication.

    [Application of reverse transcription-multiplex nested PCR to detect MLL rearrangement in AML-M4/M5].
    Pan JL, Xue YQ, Jiang HY, He J, Wang W, Wu YF.

    01/21/2010
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