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May act as a transcription factor that could act on to regulate one of the phases of hair growth.. Zusätzlich bieten wir Ihnen Hairless Proteine (5) und viele weitere Produktgruppen zu diesem Protein an.
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mammalian Hr is a phosphoprotein which can exert cross-talk with the p53 (zeige TP53 Antikörper) pathway with important implications for the regulation of cell proliferation and differentiation in tissues such as skin and brain where Hr is highly expressed.
We have identified two recurrent missense mutations in U2HR c.1A>T (p. Met1?) and c.104A>G (p.*35Wext1263*) in two Chinese Han families with Marie Unna Hereditary Hypotrichosis.
study reports two cases of Marie Unna hereditary hypotrichosis; a novel nonsense mutation of U2HR was identified in the second case, but no causative mutation in U2HR or EPS8L3 (zeige EPS8L3 Antikörper) was found in the first case
we have identified a mutation, c.74C>T, in a Chinese family with MUHH, which has been previously described in a family from Hungary. Our findings therefore indicate the prevalence of this mutation in diverse populations.
Findings indicate that hairless (HR) is a H3K9 demethylase (zeige MBD2 Antikörper) that regulates epidermal homeostasis via direct control of its target genes.
Unliganded VDR (zeige CYP27B1 Antikörper) upregulates the expression of hairless, the gene product of which acts as a downstream comodulator to feedback-repress DKKL1 (zeige DKKL1 Antikörper) and SOSTDC1 (zeige SOSTDC1 Antikörper).
deletion mutants of hairless indicate that the JmjC domain contributes to the co-repressor activity
Mutations in the gene HR coding for the hairless protein are associated with an autosomal recessive form of alopecia universalis
Marie Unna hereditary hypotrichosis is caused by a novel mutation (U2HR) in the human hairless transcript.
study reports a family with Marie Unna hereditary hypotrichosis (MUHH) from Turkey; identified the mutation c.2T > C (M1T) in all affected family members; concluded that there may be considerable clinical variations in MUHH
This study examinedthe uncommon phenotype and using microarray analyses and functional studies, we found that beta-catenin was mediated by Hr. Progenitor keratinocytes from the bulge region differentiate into both epidermis and sebaceous glands, and fail to adopt the hair keratinocytes fate in the mutant scalp, due to the decreased Wnt/beta-catenin signaling in the absence of the hairless protein.
HR regulates expression of genes in the MSX2 regulatory pathway, which explains abnormal hair follicle formation in Hr(Hp)/Hr(Hp) skin.
Hairless is required for adipocyte differentiation.
Hr loss results in a state of uncontrolled epidermal proliferation that promotes tumor development, and Hr mutant mice should no longer be considered merely hairless 'wild-type' mice
regulation of Dlx3 (zeige DLX3 Antikörper) by HR affects the IRS (zeige IARS Antikörper) keratin expression, thus modulating the formation of IRS (zeige IARS Antikörper) of hair follicle.
Foxe1 (zeige FOXE1 Antikörper) mRNA expression was suppressed in HR-overexpressing skin, as well as in HR-expressing keratinocytes.
Hr evokes an anti-apoptotic response by disrupting a p53 (zeige TP53 Antikörper) dependent pathway involving Bcl2 (zeige BCL2 Antikörper) family members.
hairless phenotype in CR rats is not allelic with mouse hairless
This thyroid hormone (zeige PTH Antikörper)-regulated corepressor associates with histone deacetylases in neonatal rat brain.
HR regulates the precise timing of Wnt (zeige WNT2 Antikörper) signaling required for hair follicle regeneration.
This gene encodes a protein that is involved in hair growth. This protein functions as a transcriptional corepressor of multiple nuclear receptors, including thyroid hormone receptor, the retinoic acid receptor-related orphan receptors and the vitamin D receptors, and it interacts with histone deacetylases. The translation of this protein is modulated by multiple regulatory ORFs that exist upstream of the primary ORF. Mutations in one of these upstream ORFs, U2HR, cause Marie Unna hereditary hypotrichosis (MUHH), an autosomal dominant form of genetic hair loss. Mutations in this gene also cause autosomal recessive congenital alopecia and atrichia with papular lesions, other diseases resulting in hair loss. Two transcript variants encoding different isoforms have been found for this gene.
, protein hairless
, hairless homolog (mouse)
, hairless protein
, protein hairless-like