Search

everythingexperts & clinicslearnfaqsresearchcommunity

for

Search:↓

This study found that ablating cyclin D3 in a Ras-dependent skin carcinogenesis model increased apoptosis in hair follicles, reducing papilloma development but potentially facilitating malignant progression when CDK6 is overexpressed.

This study identified a novel I268T mutation in the vitamin D receptor that reduces its function, contributing to hereditary vitamin D-resistant rickets, and found that a potent vitamin D analog could improve receptor function.

This study identifies a mechanism where dsRNA activates TLR3 to induce RA production, promoting hair follicle regeneration in mice and suggesting a potential role in human tissue regeneration.

This study reports on an ongoing Phase I/IIa clinical trial of ex vivo gene therapy for treating severe Recessive Dystrophic Epidermolysis Bullosa, involving six adult participants with COL7A1 mutations resulting in deficient type VII collagen production.

This study established a stable cell line for CRF1 receptor screening, which can be used to develop functional cosmetics and modulators potentially affecting hair re-growth.

This review discusses the evolution of Cereblon ligands in PROTAC technology, highlighting chemical innovations that may enhance drug-likeness and applicability in protein degradation, while noting challenges and future research directions.

This study found that mitochondrial dysfunction due to Crif1 deficiency in hair follicle stem cells significantly slows the hair growth cycle in adult mice but does not impact the maintenance of HFSC populations.

This case report identifies a novel nonsense mutation in the CDH3 gene associated with hypotrichosis and juvenile macular dystrophy.

This study found that the medication dyclonine has a potent inhibitory effect on the TRPV3 channel, effectively rescuing cell death and alleviating pruritus symptoms in a mouse model with gain-of-function TRPV3 mutations, suggesting potential for treating skin inflammation.

Diphencyprone treatment protocols could be simplified as no harm occurred despite not fully following them.

This study suggests that the HCR risk allele within the PSORS1 locus may contribute to psoriasis susceptibility by altering gene expression related to skin structure and differentiation, although these changes alone might not result in clinical symptoms.

A specific gene mutation is linked to a hereditary form of dystonia that responds well to certain medications.

This pilot clinical study introduces DEC cells as a novel therapy for Duchenne muscular dystrophy, confirming safety and efficacy in seven patients up to 24 months post-treatment.

Diphencyprone initially increases mouse hair growth, then slows it, possibly due to changes in specific protein levels.

This study suggests that the vitamin D receptor and hairless gene may directly regulate each other via a transcriptional mechanism, potentially explaining phenotypic similarities between atrichia and VDRRIIa rickets.

In this study, a patient with Cronkhite-Canada syndrome complicated by severe sepsis and disseminated intravascular coagulation was successfully treated using combined therapies, including recombinant human soluble thrombomodulin, despite the absence of a standard treatment regimen for CCS.

This study found that activating CXCR2 on ras-transformed keratinocytes promotes migration and tumor development in a mouse skin model.

This report suggests that TCDD may alter human epidermal stem cell populations by upregulating c-Myc, potentially leading to increased stem cell turnover during chloracne development.

In this retrospective case series, therapeutic responses to immunomodulatory and incretin-based therapies for Dercum's disease showed considerable individual variation, suggesting these treatments might be exploratory options when surgery isn't feasible, though further controlled studies are needed for definitive conclusions.

This article describes a method using the CUBIC protocol to clarify and visualize molecular and cellular interactions in mouse skin biopsies at single cell resolution, but does not provide new biological findings.

In this study, researchers found that overexpression of CRABP2 enhanced the proliferation of dermal papilla cells in Hu sheep through activation of the Wnt/β-catenin pathway, even when the pathway was inhibited.

This study found that a single application of TCDD on the skin of hairless mice altered epidermal differentiation, changing keratin expression patterns similarly to a known tumor promoter.

This study reported a case of hereditary vitamin D–resistant rickets caused by a single heterozygous missense mutation in the VDR gene, showing dominant-negative effects and reduced response to 1,25-dihydroxyvitamin D3.

In this study, researchers developed a new prostate cancer imaging agent, a [99m Tc]tricarbonyl complex derived from finasteride, which demonstrated high radiochemical purity and significant uptake in the prostate of a rat model, suggesting its potential for noninvasive prostate cancer imaging.

This study identified two novel mutations in the CDH3 gene causing HJMD in a Chinese patient, expanding the genetic and phenotypic understanding of the disorder.

This study reports that the DMI3 gene, essential for nodule formation in legume-rhizobial symbiosis, encodes a calcium/calmodulin-dependent protein kinase, highlighting its role in multiple plant symbioses.

This study found that deleting all three Desmoglein 1 genes in mice led to impaired skin barrier function, disorganized epidermis, and postnatal lethality, highlighting Dsg1's essential role in epidermal development and maintenance.

This study found that in a mouse model with hereditary 1,25-dihydroxyvitamin D resistant rickets, a mutant vitamin D receptor lacking hormone-binding ability could restore normal hair cycling and affect parathyroid hormone regulation.

This study provided the first X-ray crystal structure of the mammalian steroid hormone reductase AKR1D1 and identified a disease-related mutant, P133R, which may impact bile acid metabolism and cause clinical symptoms.