Редактирование: CRISPLD2

Cysteine-rich secretory protein LCCL domain-containing 2 precursor (Cysteine-rich secretory protein 11) (CRISP-11) (LCCL domain-containing cysteine-rich secretory protein 2) [CRISP11] [LCRISP2] [UNQ2914/PRO1156/PRO9783]

==Publications==

{{medline-entry
|title=A large-scale CRISPR screen and identification of essential genes in cellular senescence bypass.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31219803
|abstract=Cellular senescence is an important mechanism of autonomous tumor suppression, while its consequence such as the senescence-associated secretory phenotype (SASP) may drive tumorigenesis and age-related diseases. Therefore, controlling the cell fate optimally when encountering senescence stress is helpful for anti-cancer or anti-aging treatments. To identify genes essential for senescence establishment or maintenance, we carried out a CRISPR-based screen with a deliberately designed single-guide RNA (sgRNA) library. The library comprised of about 12,000 kinds of sgRNAs targeting 1378 senescence-associated genes selected by integrating the information of literature mining, protein-protein interaction network, and differential gene expression. We successfully detected a dozen gene deficiencies potentially causing senescence bypass, and their phenotypes were further validated with a high true positive rate. RNA-seq analysis showed distinct transcriptome patterns of these bypass cells. Interestingly, in the bypass cells, the expression of SASP genes was maintained or elevated with [[CHEK2]], [[HAS1]], or [[MDK]] deficiency; but neutralized with [[MTOR]], [[CRISPLD2]], or [[MORF4L1]] deficiency. Pathways of some age-related neurodegenerative disorders were also downregulated with [[MTOR]], [[CRISPLD2]], or [[MORF4L1]] deficiency. The results demonstrated that disturbing these genes could lead to distinct cell fates as a consequence of senescence bypass, suggesting that they may play essential roles in cellular senescence.
|mesh-terms=* CRISPR-Associated Protein 9
* CRISPR-Cas Systems
* Cell Line
* Cellular Senescence
* Fibroblasts
* Gene Expression Regulation
* Humans
* Lentivirus
|keywords=* CRISPR
* SASP
* aging
* bypass
* cellular senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6628988
}}