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Type I and Type II keratin chains can form heterodimers despite sequence differences.

Keratin heterodimers are preferred for their specific and structural advantages.

This study found that the protein hairless acts as both a corepressor and coactivator of the vitamin D receptor, influencing gene transcription in a ligand-selective manner.

In this study, rabbit esophageal epithelial cells were found to produce K4 and K13 keratins in suprabasal cells, forming disulfide-crosslinked dimers that may support the physical stability of the esophageal lining.

This study found that a novel rare variant in ITGB6 may cause intellectual disability, alopecia, and dentogingival anomalies in a specific Pakistani family, highlighting a potential role for ITGB6 beyond enamel formation.

This study presents recombinant human hair keratins K31 and K81, observing novel nanostructures from their self-assembly and emphasizing disulfide crosslinking's role in this process.

Vitamin D receptor mutations can cause alopecia by affecting hair growth genes.

This study found that in an Italian population, the HLA-DQB1*03 allele was associated with increased susceptibility to alopecia areata, particularly in cases with more than 50% hair loss.

This study found that RXRα plays a critical role in hair cycling and keratinocyte functions in mice, likely through its interaction with VDR in epidermal cells.

This study found that RXRα/RARγ heterodimers are necessary for retinoic acid-induced keratinocyte proliferation in the skin, while normal epidermal maintenance does not require RAR-mediated signaling.

This study found that vitamin D receptor activation in primary keratinocytes can occur independently of the 1,25-dihydroxyvitamin D₃ ligand, likely through interaction with retinoid X receptors.

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 demonstrated that mice lacking skin-specific RXRalpha expression developed hair follicle degeneration and alopecia, indicating the importance of RXRalpha/VDR heterodimers in maintaining hair follicle homeostasis.

This study found that a gene from hamster flank organs is indirectly regulated by androgens, despite lacking direct androgen responsive elements, indicating involvement of androgen-dependent transcription factors.

In this laboratory study, α-mangostin was found to significantly reduce melanin content and downregulate pigmentation-related genes in cultured skin and B16F10 cells, suggesting potential application as a natural whitening agent in sunscreen development.

This review discusses recent advances in understanding the structural hierarchy of trichocyte keratins, including their heterodimeric structure and distinct conformations impacting hair growth, with no new experimental results reported.

This study found that all-trans and 9-cis retinoic acids increase steroid sulfatase activity in HL60 cells through mechanisms involving RARα/RXR heterodimers and multiple signaling pathways.

This study found that in a mouse model of Ross River virus-induced joint inflammation, targeting IL-17A and IL-17A/F heterodimers reduced disease severity.

This research found that nod factor can induce root hair reorientation and gene expression in Medicago truncatula with as little as a single molecule, implicating heterotrimeric G-protein signaling in this process.

This study demonstrates a sample preparation method for wool follicles that allows for clear keratin labeling and ultrastructural preservation in microscopy, reducing common artefacts from conventional fixation techniques.

This article highlights advances in various physiological studies, including vitamin E's potential to improve aging-related outcomes in mice, but does not present new experimental results.

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 chapter discusses the molecular biology of the vitamin D receptor in gene transcription and reports no new results; it highlights recent findings on receptor activity independent of its usual ligand.

This study identified a missense mutation in the keratin 71 gene as the cause of autosomal dominant woolly hair/hypotrichosis in a Japanese family, marking the first human mutation in KRT71 linked to a hair disorder.

This study found that a novel R343H mutation in the vitamin D receptor gene impairs its transcription activity, contributing to hereditary vitamin D-resistant rickets and alopecia in the affected family.

This study identified novel isoforms of the PADI2 and PADI3 proteins, showing that PADI2β inhibits oligodendrocyte differentiation, possibly by opposing the effect of canonical PADI2, while PADI3β modulates the activity of PADI3α, suggesting new regulatory mechanisms of citrullination in tissue development.

This chapter reviews current and future strategies for identifying ligands and functions of orphan G protein-coupled receptors, but it reports no new experimental results.

This study identified new dietary ligands for the human vitamin D receptor, including curcumin and gamma-tocotrienol, which may influence its biological functions.

This article reviews the structure and regulation of the ITGB6 gene and discusses its role in integrin αvβ6 expression, with no new experimental results reported.

In this study, eight patients with hereditary vitamin D-resistant rickets who share a specific VDR mutation showed improved clinical symptoms except alopecia after up to 11 years of treatment.