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This study found that histidine decarboxylase is crucial for the hair-inducing ability of newborn mouse dermal cells, with its expression significantly decreasing in the first few days after birth.

This study found that CNGC 6, CNGC 9, and CNGC 14 are crucial for maintaining calcium oscillations necessary for normal root hair growth in plants, with mutations leading to defects like swelling and bursting.

In this study, researchers identified and examined males with 17 beta-HSD3 deficiency in a highly inbred Arab population, noting genetic findings and the progression of male characteristics despite being raised as females initially.

This study found that mutations in the PADI3 gene, which is important for hair shaft formation, may contribute to central centrifugal cicatricial alopecia among patients.

This study found that the activity of CD73, an enzyme expressed in the hair follicle epithelium, may regulate human hair growth by modulating adenosine production.

This study used developing mouse hair follicles to explore early epithelial bud formation, finding that the Rho GTPase regulator ARHGEF3 plays a crucial role in regulating cell fate and cadherin patterning, with knockouts showing disrupted morphology and increased straight hair follicle growth.

In this study, CSLD3 overexpression in Arabidopsis enhanced root and hypocotyl growth by increasing cell elongation, with root growth highly sensitive to ethylene and phosphate starvation conditions.

A gene called APCDD1, which controls hair growth, is found to be faulty in a type of hair loss called hereditary hypotrichosis simplex.

This case report identified a 6-month-old girl with congenital generalized hypertrichosis and gingival hyperplasia, where a de novo CNV on chromosome 17q24.2-24.3 was associated with reduced expression of ABCA5 and SOX9.

This study found that deleting all three Tet genes in mice led to shorter hair shafts and altered hair types, with associated changes in gene expression and DNA hydroxymethylation.

This study found that cortisone reductase deficiency is caused by inactivating mutations in the H6PD gene, affecting cortisol metabolism by preventing 11β-HSD1 enzyme function.

This study identified nine pathogenic variants in the PADI3 gene and variants in the S100A3 and TCHH genes in patients with central centrifugal cicatricial alopecia, suggesting a broader genetic basis for the disease and potential targets for genetic testing and therapies.

This study found that mice with a mutant CDP/Cux protein lacking the homeodomain showed severely impaired growth, high postnatal mortality, and reduced fertility, highlighting CDP/Cux's role in developmental regulation.

This study found that loss-of-function mutations in the HOXC13 gene cause autosomal-recessive pure hair and nail ectodermal dysplasia, emphasizing its role in hair and nail development.

This article discusses the potential genetic basis of central centrifugal cicatricial alopecia in women of African ancestry but does not provide new research results.

In this case report, a 46-year-old woman initially diagnosed with 21-hydroxylase deficiency congenital adrenal hyperplasia was later identified as having 3β-HSD2 deficiency after further investigation, highlighting the need for awareness of rarer CAH forms to prevent delayed diagnosis and insufficient treatment.

This study identified nine pathogenic variants in the PADI3 gene, and variants in the S100A3 and TCHH genes, which may disrupt protein function and contribute to central centrifugal cicatricial alopecia.

Genetic factors, especially PADI3 gene variants, contribute to CCCA in women of African descent.

In this study, researchers confirmed linkage of a form of hair-nail ectodermal dysplasia to chromosome 12 in a Pakistani family, suggesting a possible non-coding mutation in KRTHB5 or a mutation in an unknown gene.

This study found that distinct isoenzymes of 3 beta-hydroxysteroid dehydrogenase are expressed in human adrenals and gonads compared to the placenta and skin.

This study found that the mutant hairless rhino bald protein in mice interacts with the vitamin D receptor but cannot repress its transactivation and shows abnormal cellular localization.

CD73 may regulate hair growth and could be targeted for hair growth treatments.

This case report describes an instance of autosomal recessive uncombable hair syndrome caused by maternal uniparental disomy of chromosome 1.

This study found that ARHGEF3 is crucial for hair follicle development in mice, as its absence leads to defects in placode compaction and impaired follicle downgrowth, highlighting its role in regulating cell shape rearrangements during embryogenesis.

This study found that mutations in exon 3 of the hr gene are strongly associated with congenital hypotrichosis in Valle del Belice sheep, suggesting a potential genetic link to the disorder.

This study found that CYP21A2 gene mutations are the most common cause of non-classic congenital adrenal hyperplasia, while CYP11B1 mutations are rare and may partially impair enzyme activity.

A specific gene mutation causes sparse, brittle hair in a family.

In this study, prenatal ultrasonography was found to be a valuable tool for screening ectodermal dysplasia during pregnancy, and a new EDA gene variant associated with X-linked hypohidrotic ectodermal dysplasia was identified, aiding in more accurate diagnoses and reproductive decision-making.

This study identified a compound heterozygous mutation in the 3 beta-HSD gene that confirmed inherited 3 beta-HSD deficiency in a Pakistani child with salt-wasting congenital adrenal hyperplasia.