Редактирование: SHC1

SHC-transforming protein 1 (SHC-transforming protein 3) (SHC-transforming protein A) (Src homology 2 domain-containing-transforming protein C1) (SH2 domain protein C1) [SHC] [SHCA]

==Publications==

{{medline-entry
|title=Docosahexaenoic acid prevented tumor necrosis factor alpha-induced endothelial dysfunction and senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26802937
|abstract=We investigated how docosahexaenoic acid (DHA) regulated tumor necrosis factor-alpha ([[TNF]]-α)-induced senescence and dysfunction in endothelial cells (EC). We used RT-PCR to examine the expression of several genes related to senescence and dysfunction in EC. [[TNF]]-α-induced p21 protein levels were investigated by Western blot (WB) and fluorescence antibody techniques. [[TNF]]-α induced the senescence marker β-galactosidase and the expression of several senescence and endothelial dysfunction-related genes, e.g., [[CDKN1A]], [[SHC1]] and [[GLB1]]. DHA attenuated [[TNF]]-α-induced senescence-related gene expression and p21 protein expression. DHA attenuated [[TNF]]-α-induced gene expression related to dysfunction of EC, such as plasminogen activator inhibitor 1 (SERPINE1), lectin-like oxidized low-density lipoprotein receptor-1 (OLR1), thromboxane A2 receptor (TXA2R) and p38 MAPK (MAPK14). DHA reversed the [[TNF]]-α-mediated reduction of endothelial nitric oxide synthase (NOS3) gene expression. [[TNF]]-α-mediated upregulation of these genes was inhibited by allopurinol and apocynin. These results indicated that DHA regulated the expression of several genes that are associated with senescence and dysfunction of EC. 
|mesh-terms=* Cell Line
* Cellular Senescence
* Cyclin-Dependent Kinase Inhibitor p21
* Docosahexaenoic Acids
* Endothelial Cells
* Humans
* Nitric Oxide Synthase Type III
* Plasminogen Activator Inhibitor 1
* Scavenger Receptors, Class E
* Shc Signaling Adaptor Proteins
* Src Homology 2 Domain-Containing, Transforming Protein 1
* Tumor Necrosis Factor-alpha
* beta-Galactosidase
|keywords=* DHA
* Dysfunction
* Endothelial cells
* Senescence
* TNFα
|full-text-url=https://sci-hub.do/10.1016/j.plefa.2015.10.006
}}