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The cell transition from an inflammatory phase to a subsequent proliferative phase is crucial for wound healing, yet the driving mechanism remains unclear. By profiling lncRNA expression changes during human skin wound healing and screening lncRNA functions, we identified SNHG26 as a pivotal regulat...
ORGANISM(S): Homo sapiens (Human) 
2024-08-28 | PXD055231 | Pride
Keratinocyte response to SNHG26 silencing
This study aims to elucidate the mechanism by which the long non-coding RNA SNHG26 promotes fibroblast activation in keloid pathogenesis through interactions with protein partners. Using RNA pull-down coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS), we identified proteins that...
ORGANISM(S): Homo sapiens (Human) 
2026-08-13 | PXD068776 | Pride
Impaired wound healing in Snhg26 knockout mice
Analysis the transcriptome of keratinocyte after SNHG26 silencing with or without TNFa treatment for 3 hours. SNHG26 is a conseved lncRNA which is upregulated in the epidermis of human and mouse acute wound. Results of this profiling provide insight into the biological role of SNHG26 in keratinocyte...
ORGANISM(S): Homo sapiens 
2024-08-26 | GSE216823 | GEO
LncRNA SNHG26 facilitates inflammatory to proliferative state transition of keratinocyte progenitors during wound healing
Knock-down of lncRNA SNHG26 in human embryonic stem cells
The epidermal stem cell transition from inflammation to proliferation is a crucial process in tissue repair. However, the molecular mechanism underlying this process is poorly understood. Combined with lncRNA expression profiling of human acute wounds and functional screening, we identified SNHG26 a...
ORGANISM(S): Mus musculus Homo sapiens 
2024-08-26 | GSE218430 | GEO
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