CEBPD

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CEBPD
Identifiers
AliasesCEBPD, C/EBP-delta, CELF, CRP3, NF-IL6-beta, CCAAT/enhancer binding protein delta, CCAAT enhancer binding protein delta
External IDsOMIM: 116898 MGI: 103573 HomoloGene: 3808 GeneCards: CEBPD
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_005195

NM_007679

RefSeq (protein)

NP_005186

NP_031705

Location (UCSC)Chr 8: 47.74 – 47.74 MbChr 16: 15.89 – 15.89 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

CCAAT/enhancer-binding protein delta is a protein that in humans is encoded by the CEBPD gene.[5][6]

Function[]

The protein encoded by this intronless gene is a bZIP transcription factor which can bind as a homodimer to certain DNA regulatory regions. It can also form heterodimers with the related protein CEBP-alpha. The encoded protein is important in the regulation of genes involved in immune and inflammatory responses, and may be involved in the regulation of genes associated with activation and/or differentiation of macrophages.[7]

Functions[]

CEBPD is involved in regulation of apoptosis and cell proliferation. It probably acts as tumor suppressor.[8]

One study in mice showed that CEBPD prevents development of tubular injury and tubulointerstitial fibrogenesis during the progression of chronic obstructive nephropathy.[9]

Function of CEBPD gene can be effectively examined by siRNA knockdown based on an independent validation.[10]

Interactions[]

CEBPD has been shown to interact with Mothers against decapentaplegic homolog 3.[11]

See also[]

  • Ccaat-enhancer-binding proteins

References[]

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000221869 - Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000071637 - Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ Cao Z, Umek RM, McKnight SL (Sep 1991). "Regulated expression of three C/EBP isoforms during adipose conversion of 3T3-L1 cells". Genes & Development. 5 (9): 1538–52. doi:10.1101/gad.5.9.1538. PMID 1840554.
  6. ^ Williams SC, Cantwell CA, Johnson PF (Sep 1991). "A family of C/EBP-related proteins capable of forming covalently linked leucine zipper dimers in vitro". Genes & Development. 5 (9): 1553–67. doi:10.1101/gad.5.9.1553. PMID 1884998.
  7. ^ "Entrez Gene: CEBPD CCAAT/enhancer binding protein (C/EBP), delta".
  8. ^ Gery S, Tanosaki S, Hofmann WK, Koppel A, Koeffler HP (Feb 2005). "C/EBPdelta expression in a BCR-ABL-positive cell line induces growth arrest and myeloid differentiation". Oncogene. 24 (9): 1589–97. doi:10.1038/sj.onc.1208393. PMID 15674331.
  9. ^ Duitman J, Borensztajn KS, Pulskens WP, Leemans JC, Florquin S, Spek CA (Jan 2014). "CCAAT-enhancer binding protein delta (C/EBPδ) attenuates tubular injury and tubulointerstitial fibrogenesis during chronic obstructive nephropathy". Laboratory Investigation; A Journal of Technical Methods and Pathology. 94 (1): 89–97. doi:10.1038/labinvest.2013.127. PMID 24247561.
  10. ^ Munkácsy, Gyöngyi; Sztupinszki, Zsófia; Herman, Péter; Bán, Bence; Pénzváltó, Zsófia; Szarvas, Nóra; Győrffy, Balázs (2016). "Validation of RNAi Silencing Efficiency Using Gene Array Data shows 18.5% Failure Rate across 429 Independent Experiments". Molecular Therapy: Nucleic Acids. 5 (9): e366. doi:10.1038/mtna.2016.66. ISSN 2162-2531. PMC 5056990. PMID 27673562.
  11. ^ Choy L, Derynck R (Mar 2003). "Transforming growth factor-beta inhibits adipocyte differentiation by Smad3 interacting with CCAAT/enhancer-binding protein (C/EBP) and repressing C/EBP transactivation function". The Journal of Biological Chemistry. 278 (11): 9609–19. doi:10.1074/jbc.M212259200. PMID 12524424.

Further reading[]

External links[]

  • Human CEBPD genome location and CEBPD gene details page in the UCSC Genome Browser.
  • CEBPD+protein,+human at the US National Library of Medicine Medical Subject Headings (MeSH)

This article incorporates text from the United States National Library of Medicine, which is in the public domain.



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