Mouse models of alopecia: identifying structural genes that are baldly needed.
The mature hair follicle undergoes a unique developmental cycle, in which phases of growth are interspersed with phases of involution and rest. The main effectors of this cycle are skin epithelial stem cells that reside in a specialized compartment of the follicle. Defects in this cycle, or in the structure of the hair produced, often result in alopecia (partial or complete hair loss), a condition that affects a significant fraction of the population. Here we discuss transgenic mouse models that exhibit alopecia as a primary phenotype, resulting from the inactivation of genes encoding structural proteins.
Tong
Xuemei
X
Dept of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Coulombe
Pierre A
PA
D000505:Alopecia / Q000235:genetics* / Q000503:physiopathology; D000818:Animals; D002403:Cathepsins / Q000235:genetics; D015815:Cell Adhesion Molecules / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D051858:Forkhead Transcription Factors; D018859:Hair Follicle / Q000254:growth & development* / Q000473:pathology; D018398:Homeodomain Proteins / Q000235:genetics; D007633:Keratins / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D023421:Models, Animal; D014157:Transcription Factors / Q000235:genetics
D015815:Cell Adhesion Molecules; D004268:DNA-Binding Proteins; D051858:Forkhead Transcription Factors; D018398:Homeodomain Proteins; C485834:Hoxc13 protein, mouse; D014157:Transcription Factors; C090140:Whn protein; D007633:Keratins; D002403:Cathepsins