 CCAAT-Enhancer-Binding Proteins
"CCAAT-Enhancer-Binding Proteins" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
A class of proteins that were originally identified by their ability to bind the DNA sequence CCAAT. The typical CCAAT-enhancer binding protein forms dimers and consists of an activation domain, a DNA-binding basic region, and a leucine-rich dimerization domain (LEUCINE ZIPPERS). CCAAT-BINDING FACTOR is structurally distinct type of CCAAT-enhancer binding protein consisting of a trimer of three different subunits.
| Descriptor ID |
D022762
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| MeSH Number(s) |
D12.776.260.108.124 D12.776.660.167 D12.776.930.127.124
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| Concept/Terms |
CCAAT-Enhancer-Binding Proteins- CCAAT-Enhancer-Binding Proteins
- CCAAT Enhancer Binding Proteins
- CAAT-Enhancer Binding Protein
- Binding Protein, CAAT-Enhancer
- CAAT Enhancer Binding Protein
- CCAAT-Enhancer-Binding Protein
- CCAAT Enhancer Binding Protein
- Nuclear Protein C-EBP
- C-EBP, Nuclear Protein
- Nuclear Protein C EBP
- C-EBP Protein
- C EBP Protein
- CAAT-Enhancer-Binding Proteins
- CAAT Enhancer Binding Proteins
- C-EBP Proteins
- C EBP Proteins
- CCAAT Sequence-Specific DNA-Binding Proteins
- CCAAT Sequence Specific DNA Binding Proteins
- C-EBP Nuclear Protein
- C EBP Nuclear Protein
- Nuclear Protein, C-EBP
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Below are MeSH descriptors whose meaning is more general than "CCAAT-Enhancer-Binding Proteins".
Below are MeSH descriptors whose meaning is more specific than "CCAAT-Enhancer-Binding Proteins".
This graph shows the total number of publications written about "CCAAT-Enhancer-Binding Proteins" by people in this website by year, and whether "CCAAT-Enhancer-Binding Proteins" was a major or minor topic of these publications.
To see the data from this visualization as text, click here.
| Year | Major Topic | Minor Topic | Total |
|---|
| 1988 | 1 | 0 | 1 | | 1990 | 1 | 0 | 1 | | 1992 | 0 | 1 | 1 | | 1993 | 1 | 0 | 1 | | 1994 | 1 | 0 | 1 | | 1996 | 0 | 2 | 2 | | 1999 | 0 | 1 | 1 | | 2000 | 2 | 2 | 4 | | 2003 | 1 | 0 | 1 | | 2004 | 1 | 0 | 1 | | 2006 | 0 | 1 | 1 | | 2007 | 1 | 0 | 1 | | 2008 | 1 | 1 | 2 | | 2009 | 0 | 3 | 3 | | 2011 | 0 | 3 | 3 | | 2013 | 0 | 2 | 2 | | 2014 | 0 | 1 | 1 | | 2016 | 1 | 0 | 1 |
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Below are the most recent publications written about "CCAAT-Enhancer-Binding Proteins" by people in Profiles.
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Bertolino E, Reinitz J. The analysis of novel distal Cebpa enhancers and silencers using a transcriptional model reveals the complex regulatory logic of hematopoietic lineage specification. Dev Biol. 2016 May 01; 413(1):128-44.
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Godley LA. Inherited predisposition to acute myeloid leukemia. Semin Hematol. 2014 Oct; 51(4):306-21.
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Pan HC, Yang CN, Hung YW, Lee WJ, Tien HR, Shen CC, Sheehan J, Chou CT, Sheu ML. Reciprocal modulation of C/EBP-a and C/EBP-ß by IL-13 in activated microglia prevents neuronal death. Eur J Immunol. 2013 Nov; 43(11):2854-65.
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Davis KL, Marina N, Arber DA, Ma L, Cherry A, Dahl GV, Heerema-McKenney A. Pediatric acute myeloid leukemia as classified using 2008 WHO criteria: a single-center experience. Am J Clin Pathol. 2013 Jun; 139(6):818-25.
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Xu H, Yang W, Perez-Andreu V, Devidas M, Fan Y, Cheng C, Pei D, Scheet P, Burchard EG, Eng C, Huntsman S, Torgerson DG, Dean M, Winick NJ, Martin PL, Camitta BM, Bowman WP, Willman CL, Carroll WL, Mullighan CG, Bhojwani D, Hunger SP, Pui CH, Evans WE, Relling MV, Loh ML, Yang JJ. Novel susceptibility variants at 10p12.31-12.2 for childhood acute lymphoblastic leukemia in ethnically diverse populations. J Natl Cancer Inst. 2013 May 15; 105(10):733-42.
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Hickey CJ, Schwind S, Radomska HS, Dorrance AM, Santhanam R, Mishra A, Wu YZ, Alachkar H, Maharry K, Nicolet D, Mrózek K, Walker A, Eiring AM, Whitman SP, Becker H, Perrotti D, Wu LC, Zhao X, Fehniger TA, Vij R, Byrd JC, Blum W, Lee LJ, Caligiuri MA, Bloomfield CD, Garzon R, Marcucci G. Lenalidomide-mediated enhanced translation of C/EBPa-p30 protein up-regulates expression of the antileukemic microRNA-181a in acute myeloid leukemia. Blood. 2013 Jan 03; 121(1):159-69.
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Arita K, Isogai S, Oda T, Unoki M, Sugita K, Sekiyama N, Kuwata K, Hamamoto R, Tochio H, Sato M, Ariyoshi M, Shirakawa M. Recognition of modification status on a histone H3 tail by linked histone reader modules of the epigenetic regulator UHRF1. Proc Natl Acad Sci U S A. 2012 Aug 07; 109(32):12950-5.
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Metzeler KH, Becker H, Maharry K, Radmacher MD, Kohlschmidt J, Mrózek K, Nicolet D, Whitman SP, Wu YZ, Schwind S, Powell BL, Carter TH, Wetzler M, Moore JO, Kolitz JE, Baer MR, Carroll AJ, Larson RA, Caligiuri MA, Marcucci G, Bloomfield CD. ASXL1 mutations identify a high-risk subgroup of older patients with primary cytogenetically normal AML within the ELN Favorable genetic category. Blood. 2011 Dec 22; 118(26):6920-9.
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Tormos KV, Anso E, Hamanaka RB, Eisenbart J, Joseph J, Kalyanaraman B, Chandel NS. Mitochondrial complex III ROS regulate adipocyte differentiation. Cell Metab. 2011 Oct 05; 14(4):537-44.
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Odenike O, Thirman MJ, Artz AS, Godley LA, Larson RA, Stock W. Gene mutations, epigenetic dysregulation, and personalized therapy in myeloid neoplasia: are we there yet? Semin Oncol. 2011 Apr; 38(2):196-214.
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