| pubmed-article:16702408 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16702408 | lifeskim:mentions | umls-concept:C0221971 | lld:lifeskim |
| pubmed-article:16702408 | lifeskim:mentions | umls-concept:C0524627 | lld:lifeskim |
| pubmed-article:16702408 | lifeskim:mentions | umls-concept:C1416728 | lld:lifeskim |
| pubmed-article:16702408 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16702408 | pubmed:dateCreated | 2006-5-16 | lld:pubmed |
| pubmed-article:16702408 | pubmed:abstractText | Mammalian hair follicles cycle between stages of rapid growth (anagen) and metabolic quiescence (telogen) throughout life. Transition from anagen to telogen involves an intermediate stage, catagen, consisting of a swift, apoptosis-driven involution of the lower half of the follicle. How catagen is coordinated, and spares the progenitor cells needed for anagen re-entry, is poorly understood. Keratin 17 (K17)-null mice develop alopecia in the first week post-birth, correlating with hair shaft fragility and untimely apoptosis in the hair bulb. Here we show that this abnormal apoptosis reflects premature entry into catagen. Of the proapoptotic challenges tested, K17-null skin keratinocytes in primary culture are selectively more sensitive to TNFalpha. K17 interacts with TNF receptor 1 (TNFR1)-associated death domain protein (TRADD), a death adaptor essential for TNFR1-dependent signal relay, suggesting a functional link between this keratin and TNFalpha signaling. The activity of NF-kappaB, a downstream target of TNFalpha, is increased in K17-null skin. We also find that TNFalpha is required for a timely anagen-catagen transition in mouse pelage follicles, and that its ablation partially rescues the hair cycling defect of K17-null mice. These findings identify K17 and TNFalpha as two novel and interdependent regulators of hair cycling. | lld:pubmed |
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| pubmed-article:16702408 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16702408 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16702408 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16702408 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16702408 | pubmed:month | May | lld:pubmed |
| pubmed-article:16702408 | pubmed:issn | 0890-9369 | lld:pubmed |
| pubmed-article:16702408 | pubmed:author | pubmed-author:CoulombePierr... | lld:pubmed |
| pubmed-article:16702408 | pubmed:author | pubmed-author:TongXuemeiX | lld:pubmed |
| pubmed-article:16702408 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16702408 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16702408 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:16702408 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16702408 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16702408 | pubmed:pagination | 1353-64 | lld:pubmed |
| pubmed-article:16702408 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:16702408 | pubmed:meshHeading | pubmed-meshheading:16702408... | lld:pubmed |
| pubmed-article:16702408 | pubmed:meshHeading | pubmed-meshheading:16702408... | lld:pubmed |
| pubmed-article:16702408 | pubmed:meshHeading | pubmed-meshheading:16702408... | lld:pubmed |
