ArticleGenes & development2006
Keratin 17 modulates hair follicle cycling in a TNFalpha-dependent fashion.
Article in Genes & development, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
84 citing papers in PubMed, 170 citations in OpenAlex.
- Genetic mutations in Chinese patients with steatocystoma multiplex and mechanistic investigation ofJAAD international · 2026Article
- Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026Review
- Article
- Structure and function of the keratin 17 tail domain associated with keratin intermediate filament organization.European journal of cell biology · 2025Article
- Lifting regenerative barriers promotes epithelial cell fate plasticity supporting lineage conversion.Nature communications · 2025Article
- Cell death as an architect of adult skin stem cell niches.Cell death and differentiation · 2024Review
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- Th22 is the effector cell of thymosin β15-induced hair regeneration in mice.Inflammation and regeneration · 2024Article
- Autophagy critically controls skin inflammation and apoptosis-induced stem cell activation.Autophagy · 2023Article
- KRT17 from skin cells with high glucose stimulation promotes keratinocytes proliferation and migration.Frontiers in endocrinology · 2023Article
- Construction of transcriptome atlas of white yak hair follicle during anagen and catagen using single-cell RNA sequencing.BMC genomics · 2022Article
- Keratin-mediated hair growth and its underlying biological mechanism.Communications biology · 2022Article
- Article
- Advances in molecular pathogenesis of hidradenitis suppurativa: Dysregulated keratins and ECM signaling.Seminars in cell & developmental biology · 2022Review
- 4-Aminopyridine Induces Nerve Growth Factor to Improve Skin Wound Healing and Tissue Regeneration.Biomedicines · 2022Article
- A probabilistic Boolean model on hair follicle cell fate regulation by TGF-β.Biophysical journal · 2022Article
- Promoter Methylation Changes inInternational journal of molecular sciences · 2022Article
- Dissecting the Oncogenic Roles of Keratin 17 in the Hallmarks of Cancer.Cancer research · 2022Article
- Whole exome sequencing in Alopecia Areata identifies rare variants in KRT82.Nature communications · 2022Article
- Identification of key genes and signaling pathways related to Hetian sheep wool density by RNA-seq technology.PloS one · 2022Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.