| First Author | Bhattacharya S | Year | 2015 |
| Journal | J Invest Dermatol | Volume | 135 |
| Issue | 11 | Pages | 2593-2602 |
| PubMed ID | 26176759 | Mgi Jnum | J:226335 |
| Mgi Id | MGI:5697104 | Doi | 10.1038/jid.2015.281 |
| Citation | Bhattacharya S, et al. (2015) Transcription Factor CTIP2 Maintains Hair Follicle Stem Cell Pool and Contributes to Altered Expression of LHX2 and NFATC1. J Invest Dermatol 135(11):2593-602 |
| abstractText | Transcription factor CTIP2 (chicken ovalbumin upstream promoter transcription factor-interacting protein 2), also known as BCL11B, is expressed in hair follicles (HFs) of embryonic and adult skin. Ctip2-null mice exhibit reduced HF density during embryonic development. In contrast, conditional inactivation of Ctip2 in the epidermis (Ctip2(ep-/-)mice) leads to a shorter telogen and a premature entry into anagen during the second phase of hair cycling without a detectable change in the number of HFs. Keratinocytes of the bulge stem cells (SCs) niche of Ctip2(ep-/-) mice proliferate more and undergo reduced apoptosis compared with the corresponding cells of wild-type mice. However, premature activation of follicular SCs in mice lacking CTIP2 leads to the exhaustion of this SC compartment in comparison with Ctip2(L2/L2) mice, which retained quiescent follicle SCs. CTIP2 modulates expression of genes encoding EGFR and NOTCH1 during formation of HFs and those encoding nuclear factor of activated T-cells cytoplasmic calcineurin-dependent 1 and LIM homeobox 2 during normal hair cycling in adult skin. The expression of most of these genes is disrupted in mice lacking CTIP2, and these alterations may underlie the phenotype of Ctip2-null and Ctip2(ep-/-) mice. CTIP2 appears to serve as a transcriptional organizer that integrates input from multiple signaling cues during HF morphogenesis and hair cycling. |
