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This study found that selectively inactivating ribonucleotide excision repair in mouse epidermis leads to DNA damage, keratinocyte intraepithelial neoplasia, and squamous cell carcinoma, indicating a potential tumor-promoting mechanism related to compromised genome maintenance.

In this study, researchers found that selectively disabling ribonucleotide excision repair in mouse epidermis caused DNA damage, skin inflammation, and led to skin cancer, suggesting a potential role for this repair mechanism in tumorigenesis.

This study reviews the role of the zinc finger protein CXXC5 in cellular signaling and its implications for cancer, discussing how its dysregulation is linked to various physiological and pathological processes, as well as potential therapies targeting CXXC5.

This study identified a novel KRT86 mutation associated with autosomal dominant monilethrix, expanding understanding of its genetic basis beyond known motifs.

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.

This study identified a genetic locus associated with rhabdomyosarcoma susceptibility in mice and found that specific differentiation markers are linked to the regression of basal cell carcinoma.

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.

This study found that the mammalian Hr protein can interact with the p53 pathway by binding to a specific p53 response element, influencing the regulation of genes involved in cell cycle control.

Mutations in β1 integrins cause embryonic death but have milder effects on skin.

This study found that the Arabidopsis thaliana protein Formin 2 localizes to plasmodesmata and is crucial for regulating their permeability by anchoring actin filaments, which affects virus susceptibility.

This abstract reviews the role of the human KRT 16 wild-type allele in skin and hair development and its association with certain genetic skin disorders, without presenting new findings.

In this study, conditional inactivation of the Mad2l1 SAC gene in mice led to aggressive and lethal acute lymphoblastic leukemia and hepatocellular carcinoma, demonstrating a link between chromosomal instability and cancer development.

In this study, researchers identified the c.296C>T (p.T99I) variant in the KRT32 gene, which co-segregates with loose anagen hair syndrome, and found it decreases binding affinity to KRT82, potentially weakening hair anchorage.

This study found that a heterozygous missense mutation in ATR is associated with a hereditary cancer syndrome, manifested by oropharyngeal cancer and other anomalies, in an autosomal-dominant inheritance pattern across a five-generation family.

This study found that selective inactivation of ribonucleotide excision repair in mouse epidermis led to spontaneous DNA damage, skin inflammation, and the development of squamous cell carcinoma, suggesting potential implications for cancer development in humans.

PRSS35 enzyme may help start skin tumors and could be a target for cancer treatment.

This study found that loss of Ptch1 function in mouse skin's basal cells is sufficient to rapidly induce tumors resembling human basal cell carcinoma, suggesting Ptch1 as a key tumor suppressor.

This study developed a new STR typing strategy for forensic casework, enabling the simultaneous analysis of 11 polymorphic systems, particularly useful for limited or degraded DNA samples such as telogen hair roots.

This study found that RSPO1 mutations in patients with a 46XX disorder of sexual development contribute to impaired skin integrity and increased risk of squamous cell carcinoma in areas subject to friction.

This study found that the simultaneous inactivation of pRb and p53 genes in mouse epidermis accelerated aggressive squamous cell carcinoma development via activation of the epidermal growth factor receptor/Akt pathway.

This study found that Rap1 deficiency in mice may lead to telomere shortening, DNA damage, and impaired mitochondrial function, contributing to cardiac aging and dysfunction.

This study found that BRG1 is crucial for keratinocyte migration during skin wound healing, as its suppression impairs wound closure by inhibiting migration without affecting cell proliferation or apoptosis.

In this study, researchers found that K17−/− mice suffered more severe hair follicle damage but showed reduced epidermal inflammation after ionizing radiation, with K17's absence leading to aberrant cell cycle progression due to altered p53 genome binding and reduced B-Myb degradation.

This study identifies a mechanism where dsRNA activates TLR3 to induce RA production, promoting hair follicle regeneration in mice and suggesting a potential role in human tissue regeneration.

This study found that Krtap11-1 may play an important role in keratin-bundle assembly in the hair cortex, influencing the physical properties of hair.

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.

This study suggests that the interaction between folliculin and plakophilin-4 (p0071) may play a role in folliculin's tumor suppressor function by regulating RhoA signaling, impacting cell migration and junction formation.

This study found that TRM21 acts as a positive regulator of flavonoid biosynthesis at the translational level in Arabidopsis, leading to changes in root hair growth and a decrease in flavonoid content when TRM21 is mutated.

This study identified a mutation in the keratin 71 gene that causes curly hair in certain rats, advancing our understanding of hair formation.