ArticleThe Biochemical journal2002
COUP-TF (chicken ovalbumin upstream promoter transcription factor)-interacting protein 1 (CTIP1) is a sequence-specific DNA binding protein.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.
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Who cites it
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- Common genetic variation in the 3'-BCL11B gene desert is associated with carotid-femoral pulse wave velocity and excess cardiovascular disease risk: the AortaGen Consortium.Circulation. Cardiovascular genetics · 2012Pooled it
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- The transcription factor Bcl11a is essential for B-1a cell maintenance during aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Advances in the molecular mechanisms of zinc-finger transcription factors in neurodevelopmental disorders.IBRO neuroscience reports · 2025Review
- Multimeric transcription factor BCL11A utilizes two zinc-finger tandem arrays to bind clustered short sequence motifs.Nature communications · 2025Article
- Targeting BCL11B in CAR-engineered lymphoid progenitors drives NK-like cell development with prolonged anti-leukemic activity.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
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- Dual role ofBlood science (Baltimore, Md.) · 2024Review
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- Transcriptional Repressor BCL11A in Erythroid Cells.Advances in experimental medicine and biology · 2024Review
- A Bcl11bFrontiers in immunology · 2024Article
- Deciphering clinical significance of BCL11A isoforms and protein expression roles in triple-negative breast cancer subtype.Journal of cancer research and clinical oncology · 2023Article
- Bcl11b sustains multipotency and restricts effector programs of intestinal-resident memory CD8Science immunology · 2023Article
- The Drosophila homologue of CTIP1 (Bcl11a) and CTIP2 (Bcl11b) regulates neural stem cell temporal patterning.Development (Cambridge, England) · 2022Article
- Transcription factors Bcl11a and Bcl11b are required for the production and differentiation of cortical projection neurons.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway.EMBO reports · 2022Article
- Identification of two novel variants of theFrontiers in molecular neuroscience · 2022Article
- BCL11B depletion induces the development of highly cytotoxic innate T cells out of IL-15 stimulated peripheral blood αβ CD8+ T cells.Oncoimmunology · 2022Article
36 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chicken ovalbumin upstream promoter transcription factor (COUP-TF)-interacting proteins 1 and 2 [CTIP1/Evi9/B cell leukaemia (Bcl) l1a and CTIP2/Bcl11b respectively] are highly related C(2)H(2) zinc finger proteins that are abundantly expressed in brain and the immune system, and are associated with immune system malignancies. A selection procedure was employed to isolate high-affinity DNA binding sites for CTIP1. The core binding site on DNA identified in these studies, 5'-GGCCGG-3' (upper strand), is highly related to the canonical GC box and was bound by a CTIP1 oligomeric complex(es) in vitro. Furthermore, both CTIP1 and CTIP2 repressed transcription of a reporter gene harbouring a multimerized CTIP binding site, and this repression was neither reversed by trichostatin A (an inhibitor of known class I and II histone deacetylases) nor stimulated by co-transfection of a COUP-TF family member. These results demonstrate that CTIP1 is a sequence-specific DNA binding protein and a bona fide transcriptional repressor that is capable of functioning independently of COUP-TF family members. These findings may be relevant to the physiological and/or pathological action(s) of CTIPs in cells that do not express COUP-TF family members, such as cells of the haematopoietic and immune systems.
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