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iRhom2(Uncv) mutation blocks bulge stem cells assuming the fate of hair follicle

机译:假设毛囊的命运,iRhom2(Uncv)突变可阻止膨大的干细胞

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iRhom2 is necessary for maturation of TNF alpha-converting enzyme, which is required for the release of tumor necrosis factor. In the previous study, we found that the iRhom2(Uncv) mutation in N-terminal cytoplasmic domain-encoding region (iRhom2(Uncv)) leads to aberrant hair shaft and inner root sheath differentiation, thus results in a hairless phenotype in homozygous iRhom2(Uncv/Uncv) BALB/c mice. In this study, we found iRhom2 mutation decreased hair matrix proliferation, however, iRhom2(Uncv/Uncv) mice displayed hyperproliferation and hyperkeratosis in the interfollicular epidermis along with hypertrophy in the sebaceous glands. The number of bulge SCs was not altered and the hair follicle cycle is normal in iRhom2(Uncv/Uncv) mice. The decreased proliferation in hair matrix but increased proliferation in epidermis and sebaceous glands in iRhom2 mice may implying that iRhom2(Uncv) mutation blocks bugle stem cells assuming the fate of hair follicle. This study identifies iRhom2 as a novel regulator for determination of keratinocyte lineages.
机译:iRhom2对于TNFα转换酶的成熟是必需的,这是释放肿瘤坏死因子所必需的。在先前的研究中,我们发现N末端胞质域编码区(iRhom2(Uncv))中的iRhom2(Uncv)突变导致异常的毛干和内根鞘分化,从而导致纯合iRhom2( Uncv / Uncv)BALB / c小鼠。在这项研究中,我们发现iRhom2突变降低了毛发基质的增殖,但是,iRhom2(Uncv / Uncv)小鼠在小泡间表皮中表现出过度增殖和过度角化以及皮脂腺中的肥大。在iRhom2(Uncv / Uncv)小鼠中,膨大的SC的数量没有改变,毛囊周期正常。在iRhom2小鼠中,毛发基质的增殖减少,但表皮和皮脂腺的增殖增加,这可能意味着iRhom2(Uncv)突变假定了毛囊的命运会阻止军号干细胞。这项研究确定iRhom2作为确定角质形成细胞谱系的新型调节剂。

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