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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 mimicking the XPD point mutation in mice resulted in trichothiodystrophy-like symptoms, supporting the role of basal transcription and DNA repair defects in the disease.

In this study, mice engineered to express human EGFR showed tissue-specific growth defects and neurodegeneration rescue, but developed severe heart issues and accelerated bone cell differentiation.

This study observed that PCR-based genotyping for cre-loxP mice can lead to errors due to cre-mediated recombination in non-target tissues like tails, affecting the detection of lox alleles.

This study found that the PP2A-B55α regulatory subunit is crucial for ectodermal development in mice, with knockout embryos displaying severe neural and epidermal defects and failing to survive to birth.

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 the tetracycline-regulated transcription system effectively controls conditional gene expression in the mouse epidermis, allowing suppression and activation of specific genes with doxycycline.

This study reported that overexpressing ornithine decarboxylase in C57Bl/6 mice increased their sensitivity to tumor promotion by TPA, a change reversible by doxycycline treatment.

This study investigated dual TCR Treg cells in mouse tissues, revealing a high proportion and diverse pairing patterns compared to single TCR Tregs, providing insights into their origins and characteristics across different tissue locations.

In this study, researchers analyzed over 5,000 T cells per sample using scRNA+TCR-seq technology and found that dual TCR Tregs are present in high proportions across various mouse tissues, showing unique TCR pairing patterns, V(D)J usage, and mRNA expression compared to single TCR Tregs.

This study suggests that inducible transgenic mice showing hair follicle changes similar to telogen effluvium in humans might serve as a useful model for understanding this type of hair loss.

This study analyzed skin from 538 knockout mouse mutants and identified 50 with epidermal phenotypes, providing valuable insights into genetic conditions and systemic effects related to skin abnormalities.

This study found that mice with a disrupted TGFα gene display a curly whisker-coat phenotype, similar to waved-1 mice, suggesting TGFα's crucial role in skin architecture and hair development.

This study observed that knocking out the 1α-hydroxylase gene in mice resulted in rickets and growth retardation, demonstrating the enzyme's crucial role in vitamin D function in animals.

This study identifies iRhom2 as a crucial regulator of hair follicle differentiation, showing that the iRhom2Uncv mutation leads to dysplasia and reduced TACE maturation, resulting in a hairless phenotype in mice.

This study found that removing PPARγ specifically from mouse adipose tissue led to severe fat loss, insulin resistance, diabetes, and associated metabolic abnormalities.

This study successfully established Tsc2-deficient embryonic stem cells from Eker rats and found these cells have distinct gene expression compared to non-mutant cells, which could help identify new therapeutic targets for TSC-related pathogenesis.

This study found that homozygous mutant mice with a hypomorphic CD18 mutation developed a chronic inflammatory skin disease resembling human psoriasis, potentially implicating additional genetic factors in disease susceptibility.

In this study, 25% of CCHCR1-deficient mice exposed to stress developed hair loss similar to human alopecia areata, suggesting CCHCR1 is a susceptibility gene for the disease.

PTHrP is important for bone formation and may be targeted for osteoporosis treatment and longevity therapies.

This study identified the Itpr3 gene as responsible for the tufted hair loss phenotype in the BTBR mouse strain.

This study demonstrated that mitochondrial function in keratinocytes is crucial for maintaining skin homeostasis and hair follicle development, as its impairment led to disrupted hair morphogenesis and early death in mice.

This study found that Acvr1b signaling is crucial for both hair follicle development and cycling in mice, with the genetic disruption leading to hair loss and a thickened epidermis.

In this study, researchers observed that dormant TRP-2+ melanoma cells in bone marrow can interact with CD8+ T cells in tumor-bearing ret transgenic mice, potentially influencing immune responses.

In this study, researchers created a mutant mouse lacking the first cut repeat in the Cux/CDP protein, resulting in curly vibrissae and wavy hair, supporting the role of Cux/CDP's DNA binding domains in gene regulation during development.

This study found that conditional deletion of CD271 in mouse epidermis led to significant disorganization and increased thickness, suggesting CD271's crucial role in regulating skin differentiation and structure.

This study identified the rough coat mutation in mice, but found that LOXL is not the causal gene, although its downregulation might contribute to related phenotypic changes.

Researchers created a new mouse model for studying scleroderma.

In this study, researchers developed a new photoactivatable Cre recombinase mouse model, DiLiCre, which allows precise light-induced genetic modifications and cell tracing, demonstrating its effectiveness for advancing biological and biomedical research.