<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tang L</submitter><funding>Guangdong Provincial Hospital of Chinese Medicine</funding><funding>The 2020 Guangdong Provincial Science and Technology Innovation Strategy Special Fund</funding><funding>Administration of Traditional Chinese Medicine of Guangdong Province</funding><funding>Specific Fund of State Key Laboratory of Dampness Syndrome of Chinese Medicine</funding><funding>National Natural Science Foundation of China</funding><funding>Natural Science Foundation of Guangdong Province</funding><funding>Guangdong College of Traditional Chinese Medicine</funding><pagination>282-291</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11439983</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36(5)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Excessive growth of keratinocytes is the critical event in the etiology of psoriasis. However, the underlying molecular mechanism of psoriatic keratinocyte hyperproliferation is still unclear.&lt;h4>Objective&lt;/h4>This study aimed to figure out the potential contributory role of S-phase kinase-associated protein 2 (SKP2) in promoting the hyperproliferation of keratinocytes in psoriasis.&lt;h4>Methods&lt;/h4>We analyzed microarray data (GSE41662) to investigate the gene expression of &lt;i>SKP2&lt;/i> in psoriatic lesion skins compared with their adjacent non-lesional skin. Then, we further confirmed the mRNA and protein expression of SKP2 in human psoriatic skin tissues, imiquimod (IMQ)-induced psoriatic mice back skins and tumor necrosis factor α (TNF-α), interleukin (IL)-17A and IL-6-</pubmed_abstract><journal>Annals of dermatology</journal><pubmed_title>Upregulated SKP2 Empowers Epidermal Proliferation Through Downregulation of P27 Kip1.</pubmed_title><pmcid>PMC11439983</pmcid><funding_grant_id>YN2024HL04</funding_grant_id><funding_grant_id>SZ2021ZZ23</funding_grant_id><funding_grant_id>YN2018QJ03</funding_grant_id><funding_grant_id>82004377</funding_grant_id><funding_grant_id>2020B1212030006</funding_grant_id><funding_grant_id>2024A1515030148</funding_grant_id><funding_grant_id>20222066</funding_grant_id><funding_grant_id>SZ2022QN10</funding_grant_id><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Zheng X</pubmed_authors><pubmed_authors>Li C</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Huang H</pubmed_authors><pubmed_authors>Han W</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Wu D</pubmed_authors><pubmed_authors>Feng B</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Dai Z</pubmed_authors><pubmed_authors>Wang M</pubmed_authors><pubmed_authors>Tang L</pubmed_authors><pubmed_authors>Qiu X</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Su Z</pubmed_authors><pubmed_authors>Zheng G</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Upregulated SKP2 Empowers Epidermal Proliferation Through Downregulation of P27 Kip1.</name><description>&lt;h4>Background&lt;/h4>Excessive growth of keratinocytes is the critical event in the etiology of psoriasis. However, the underlying molecular mechanism of psoriatic keratinocyte hyperproliferation is still unclear.&lt;h4>Objective&lt;/h4>This study aimed to figure out the potential contributory role of S-phase kinase-associated protein 2 (SKP2) in promoting the hyperproliferation of keratinocytes in psoriasis.&lt;h4>Methods&lt;/h4>We analyzed microarray data (GSE41662) to investigate the gene expression of &lt;i>SKP2&lt;/i> in psoriatic lesion skins compared with their adjacent non-lesional skin. Then, we further confirmed the mRNA and protein expression of SKP2 in human psoriatic skin tissues, imiquimod (IMQ)-induced psoriatic mice back skins and tumor necrosis factor α (TNF-α), interleukin (IL)-17A and IL-6-</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-05-22T03:13:41.891Z</modification><creation>2025-04-06T22:17:08.45Z</creation></dates><accession>S-EPMC11439983</accession><cross_references><pubmed>39343755</pubmed><doi>10.5021/ad.23.118</doi></cross_references></HashMap>