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This review explores the immunological aspects of epidermal differentiation in loricrin knockout mice, offering insights into keratinization and potential intrinsic factors affecting immune function, but provides no new clinical findings.

This study found that mice with a homozygous knockout of the Ten1 gene, developed through CRISPR-Cas9-mediated exon 3 deletion, exhibited telomere shortening and symptoms consistent with accelerated aging, such as reduced lifespan, skin changes, aplastic anemia, and cerebellar hypoplasia.

In this study using tamoxifen-inducible claudin-1 knockout mice, researchers observed that tight junction barrier leakage induced stratum corneum barrier defects and skin inflammation, suggesting a possible cycle of barrier damage and inflammation in atopic dermatitis.

In this study, Sept4 knockout mice showed improved wound healing and hair follicle regeneration compared to wild-type controls, suggesting potential therapeutic uses for SEPT4 inhibition.

This study found that preventing abnormal mineral ion homeostasis in vitamin D receptor knockout mice stopped bone abnormalities, while the animal's skin phenotype arose from direct receptor effects independent of vitamin D.

This study suggests that the down-regulation of 14-3-3 proteins in wild-type keratinocytes, absent in Smad4 mutant keratinocytes, might contribute to the failure of hair follicles to initiate catagen in Smad4 knockout mice.

In this study, Gsdma1/2/3 knockout mice showed reduced epidermal hyperplasia and inflammation when induced by PMA, which was attributed to decreased EGFR-Stat3/Akt signaling due to a decrease in related ligands.

In this study, inducible whole-body Acly-knockout mice revealed that ACLY is essential for skin homeostasis, as its deficiency led to increased sebum production and skin abnormalities, indicating a vital role for cytosolic acetyl-CoA synthesis in preserving skin barrier integrity and systemic lipid regulation.

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.

This study found that in mice, knockout of Rac1 and Rac3 in keratinocytes led to reduced white adipose tissue and revealed Rac-dependent paracrine pathways affecting pre-adipocyte differentiation.

In this study, researchers found that Fgf21 knockout mice exhibited delayed hair follicle cycling compared to wild-type mice, potentially due to altered miRNA interactions affecting Vezf1 and Map3k1 expression, providing insights into the molecular regulation of hair growth.

In this study, researchers created a mouse model using CRISPR/Cas9 technology to investigate hypotrichosis simplex and woolly hair, finding that Krt71-knockout mice exhibited curly hair and developed complete hair shedding without immune deficiencies, mimicking conditions seen in humans and potentially aiding future hair disorder research.

This study demonstrated that an AR-EGFP transgene can restore AR function and fertility in Sertoli cell-specific AR knockout mice, highlighting its potential use in understanding androgen receptor functions.

This study found that alpha mangostin protected wild-type MCF10A breast cancer cells, but not p53 knockout cells, from damage by the chemotherapy agent paclitaxel.

This study found that CD34 is necessary for TPA-induced activation of hair follicle stem cells and tumor formation in mice, with CD34 knockout mice showing delayed and reduced tumor development compared to wild-types.

This study suggests that MMP-9 plays a significant role in extracellular matrix remodeling during hair canal formation in mice, as indicated by delayed hair shaft emergence and hair canal development in MMP-9 knockout mice.

In this study, researchers identified that three homologous genes—ZmSPL10, ZmSPL14, and ZmSPL26—are crucial for the development of stigmatic papilla in maize, with triple knockout mutants lacking these genes showing almost no stigmatic papilla and significantly reduced kernel setting.

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.

This study found that overexpressing FGF22 in dermal papilla cells enhanced hair follicle stem cell proliferation and viability, while its knockout reduced these attributes, indicating its role in hair follicle regeneration.

This research suggests that hair keratins evolved from claw keratins in a hairless ancestor, with Hoxc13 controlling their expression in tetrapods, evidenced by the knockout of Hoxc13 hindering claw formation in Xenopus tropicalis frogs.

This study provides genetic evidence that desmoglein-1 can compensate for the loss of desmoglein-3 in hair adhesion, supporting the desmoglein compensation hypothesis.

In this study, the disruption of Gh/tissue transglutaminase in mice did not affect viability but reduced thymocyte viability and fibroblast adhesion, suggesting its role in cell stabilization and extracellular matrix interactions.

This study found that absence of α3 integrin in mice led to faster wound healing but also caused inflammation, hair loss, and skin defects, suggesting complex roles in skin integrity and repair.

This study found that Wnt secretion is important for skin homeostasis in mice, as Evi-deficient mice developed skin lesions resembling psoriasis and showed immune cell imbalance.

This study found that the absence of laminin α5 in adult mice's epidermal basement membrane led to keratinocyte hyperproliferation and immune cell changes, affecting hair follicle development through altered growth factor expression.

This study found that Stat3 removal in keratinocytes of mice impairs healing and disrupts the normal hair cycle, leading to skin ulcers and hair loss as they age.

Lack of TrkC receptor delays hair follicle development.

This study revealed that deleting EZH2 in mesenchyme-derived cells of the female reproductive tract led to impaired uterine gland development and pregnancy loss in mice, highlighting EZH2's crucial role in fertility.

This study found that Epiprofin acts as a negative regulator of parathyroid hormone transcription, with potential implications for controlling PTH production in hyperparathyroidism.

This study found that deleting the Twist1 gene in skin keratinocytes significantly reduced UVB-induced skin cancer and hyperproliferation in mice and suggested Twist1 as a target for skin cancer prevention.