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In this study, a novel mutation in the glucocorticoid receptor gene was identified in a young woman, impairing glucocorticoid signaling and leading to generalized glucocorticoid resistance.

A genetic mutation caused severe rickets and alopecia in an Indian patient, but high-dose calcium and phosphate treatment improved their condition.

This study reports that mutations in human L-PGDS affect the entrance and exit of ligands in its binding cavity, suggesting these residues play a role in ligand interaction processes.

This study reports the crystallization of the human androgen receptor's ligand-binding domain with nonsteroidal ligands, which may aid in understanding the differences in binding compared to steroidal ligands.

This study found that a specific VDR amino acid substitution in children with hereditary vitamin D-resistant rickets disrupts ligand binding and gene activation but does not impair hair follicle development.

This case report documents successful virilization, including penile length increase, in a boy with partial androgen insensitivity syndrome using high-dose testosterone combined with anastrozole.

This study identified a recurrent mutation in the endothelin receptor type A associated with mandibulofacial dysostosis with alopecia, and proposed a mechanism involving increased ligand affinity due to structural changes.

This study found that the effects of the vitamin D receptor on hair follicle cycling in mice are independent of its ability to bind a hormone, with specific domain mutations influencing hair regrowth outcomes.

In this case study, a girl with hereditary vitamin D resistant rickets had a novel mutation in the VDR gene that affected hair cycling without causing total alopecia, suggesting ligand-independent VDR function in hair cycling.

This study identified novel selective androgen receptor modulators with enhanced in vivo pharmacological activity through structure-activity relationship analysis in castrated rats.

This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.

This study found that hair follicle homeostasis in mice requires vitamin D receptor expression in keratinocytes, independent of its ligand activation.

This study found that a novel missense mutation in the vitamin D receptor caused hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia by disrupting protein function, highlighting the importance of DNA binding in hair development.

This study found a previously unreported ST14 gene mutation in a patient with ichthyosis-hypotrichosis syndrome, highlighting novel skin and hair characteristics and emphasizing the critical role of the Asp482 amino acid in matriptase activation.

In this study, only Vdr-knockout rats showed both abnormal skin formation and alopecia, which may provide insights into vitamin D receptor function and its role in the hair growth cycle.

In this study, FMN was found to inhibit androgen receptor function and androgen-regulated gene expression in prostate cancer cells, suggesting potential as an antiandrogen therapy.

This article reviews genetic and phenotypic aspects of androgen insensitivity syndromes, emphasizing the diversity of mutations that complicates molecular screening and the importance of genotype-phenotype correlations.

This study suggests that caribine may enhance the interaction between CRFR and maltose binding protein, potentially offering a new approach for treating hair loss.

This study identified novel 4-Amino-2H-benzo[h]chromen-2-one analogs as potent androgen receptor antagonists that show strong antiproliferative activity against prostate cancer cells, suggesting them as potential lead compounds for therapy development.

This study indicates that MAGE-11 modulates androgen receptor transcriptional activity through F-box interactions, independent of the activation function 2 pathway, revealing a novel mechanism for androgen receptor regulation.

This review discusses potential new drug treatment strategies for alopecia areata based on genome-wide association study findings, but it reports no new clinical results.

This study found that certain T cell-associated genes were upregulated in dogs with Vogt-Koyanagi-Harada syndrome and vitiligo, suggesting a shared immunopathogenesis with humans.

In this study, researchers found that ligand homodimerization controls the receptor binding specificity of the FGF9 subfamily, preventing off-target activation of FGFR "b" isoforms.

This study found that the AtSfh1 protein in Arabidopsis is essential for phosphatidylinositol-4,5-bisphosphate signaling crucial to polarized root hair growth, utilizing both phosphatidylinositol and phosphatidylcholine-binding activities.

This study used cryoelectron microscopy to unveil the structure of LPA-bound human LPAR6, revealing unique ligand binding and recognition modes distinct from LPAR1, which may aid in designing targeted compounds for hair loss and cancer.

This in-silico study identified several compounds as potential Vitamin D Receptor agonists, with Dolichosterone showing the strongest binding energy.

This review discusses AR-modulating agents developed between 2012 and 2018, highlighting challenges with ligand-binding domain antagonists and proposing nonconventional approaches targeting other domains as promising strategies.

This review summarizes structural insights into androgen receptor dynamics, highlighting its flexibility in binding numerous partners, which may explain adaptive resistance mutations in cancer and loss of function in androgen insensitivity syndrome.

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 suggests that unliganded vitamin D receptors in mice may cause more severe skeletal and mineral ion defects than VDR-null conditions, and vitamin D analogues may restore function in specific VDR mutations.