Ctip2, also known as COUP-TF interacting protein 2 or BCL11B, is a multifunctional transcription factor involved in numerous cellular physiological processes. It plays a significant role in skin development and maintenance, particularly in the regulation of the epidermal permeability barrier (EPB), wound healing, inflammatory diseases, and epithelial cancers. It also has a relatively unexplored connection with lipid metabolism control and its impact on EPB homeostasis, delayed wound healing, exacerbation of inflammatory diseases, and promotion and progression of cancer. Ctip2 controls keratinocyte proliferation and cytoskeletal organization, and regulates the onset and maintenance of differentiation in keratinocytes. It integrates keratinocyte proliferation and the switch to differentiation by directly and positively regulating EGFR transcription in proliferating cells and Notch1 transcription in differentiating cells. Ctip2 is known for its role in DNA double-strand break (DSB) repair and genome stability. It is an interacting partner of the Mre11/Rad50/Nbs1 (MRN) DNA damage sensor protein complex, which recognizes DNA double-strand breaks and promotes the resection of 5′ strands to generate 3′ single-stranded intermediates necessary for homologous recombination. Ctip2 is central to the differentiation of medium spiny neurons (MSN) and striatal development. In the absence of Ctip2, MSN do not fully differentiate, leading to severely disrupted patch-matrix organization within the striatum, which is critical in motor control and affected in diseases like Huntington's. Ctip2 is also involved in the formation of T lymphocytes, which is crucial for the immune system.
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