Редактирование: CSRP1

Cysteine and glycine-rich protein 1 (Cysteine-rich protein 1) (CRP) (CRP1) (Epididymis luminal protein 141) (HEL-141) [CSRP] [CYRP]

==Publications==

{{medline-entry
|title=[[FOXO3]], a Molecular Search for the Fountain of Youth.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30849363
|abstract=[[FOXO3]] has been consistently associated with longevity and with a reduction in the prevalence of cardiovascular disease. In this issue, Yan et al. (2019) report that [[FOXO3]]-activated vascular cells derived from human embryonic stem cells (ESCs) promote multiple vascular functions and reverse cellular aging through the transcriptional repression of [[CSRP1]].
|mesh-terms=* Adolescent
* Cellular Senescence
* Forkhead Box Protein O3
* Forkhead Transcription Factors
* Humans
* Longevity
* Regeneration

|full-text-url=https://sci-hub.do/10.1016/j.stem.2019.02.008
}}
{{medline-entry
|title=[[FOXO3]]-Engineered Human ESC-Derived Vascular Cells Promote Vascular Protection and Regeneration.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30661960
|abstract=[[FOXO3]] is an evolutionarily conserved transcription factor that has been linked to longevity. Here we wanted to find out whether human vascular cells could be functionally enhanced by engineering them to express an activated form of [[FOXO3]]. This was accomplished via genome editing at two nucleotides in human embryonic stem cells, followed by differentiation into a range of vascular cell types. [[FOXO3]]-activated vascular cells exhibited delayed aging and increased resistance to oxidative injury compared with wild-type cells. When tested in a therapeutic context, [[FOXO3]]-enhanced vascular cells promoted vascular regeneration in a mouse model of ischemic injury and were resistant to tumorigenic transformation both in vitro and in vivo. Mechanistically, constitutively active [[FOXO3]] conferred cytoprotection by transcriptionally downregulating [[CSRP1]]. Taken together, our findings provide mechanistic insights into [[FOXO3]]-mediated vascular protection and indicate that [[FOXO3]] activation may provide a means for generating more effective and safe biomaterials for cell replacement therapies.
|mesh-terms=* Adult
* Animals
* Cell Differentiation
* Disease Models, Animal
* Embryonic Stem Cells
* Endothelial Cells
* Forkhead Box Protein O3
* Genetic Engineering
* Humans
* Ischemia
* Male
* Mice
* Mice, Inbred BALB C
* Mice, Inbred NOD
* Mice, Nude
* Mice, SCID
* Regeneration
|keywords=* FOXO3
* aging
* gene editing
* stem cell
* vascular cells
|full-text-url=https://sci-hub.do/10.1016/j.stem.2018.12.002
}}