<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE272nnn/GSE272102/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE272102</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Effect of Knockdown of PAXBP1 on gene expression of HaCaT keratinocytes</name><description>Here, we report that the targeted deletion of Paxbp1 in epidermal keratinocytes mediated by Keratin14-Cre leads to severe disruption in skin architecture. Mice deficient in Paxbp1 exhibited a substantially reduced epidermal thickness and pronounced separation at the dermo-epidermal junction upon birth. Mechanistically, we demonstrate that the absence of Paxbp1 hinders cellular proliferation, marked by a halt in cell cycle transition, suppressed gene expression of proliferation, and a compromised DNA replication pathway in basal keratinocytes, resulting in the thinning of skin epidermis. Moreover, molecules and pathway associated with hemidesmosome assembly were impaired in Paxbp1-deficient keratinocytes, culminating in the detachment of the skin epidermal layer. Therefore, our study highlights an indispensable role of Paxbp1 in the maintenance of epidermal homeostasis.</description><dates><publication>2026/07/01</publication></dates><accession>GSE272102</accession><cross_references><GSM>GSM8393284</GSM><GSM>GSM8393285</GSM><GSM>GSM8393286</GSM><GSM>GSM8393287</GSM><GSM>GSM8393288</GSM><GSM>GSM8393289</GSM><GPL>16791</GPL><GSE>272102</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>