Редактирование: CCAR2

Cell cycle and apoptosis regulator protein 2 (Cell division cycle and apoptosis regulator protein 2) (DBIRD complex subunit KIAA1967) (Deleted in breast cancer gene 1 protein) (DBC-1) (DBC.1) (NET35) (p30 DBC) [DBC1] [KIAA1967]

==Publications==

{{medline-entry
|title=CCAR-1 is a negative regulator of the heat-shock response in Caenorhabditis elegans.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30003683
|abstract=Defects in protein quality control during aging are central to many human diseases, and strategies are needed to better understand mechanisms of controlling the quality of the proteome. The heat-shock response (HSR) is a conserved survival mechanism mediated by the transcription factor [[HSF1]] which functions to maintain proteostasis. In mammalian cells, [[HSF1]] is regulated by a variety of factors including the prolongevity factor [[SIRT1]]. [[SIRT1]] promotes the DNA-bound state of [[HSF1]] through deacetylation of the DNA-binding domain of [[HSF1]], thereby enhancing the HSR. [[SIRT1]] is also regulated by various factors, including negative regulation by the cell-cycle and apoptosis regulator [[CCAR2]]. [[CCAR2]] negatively regulates the HSR, possibly through its inhibitory interaction with [[SIRT1]]. We were interested in studying conservation of the [[SIRT1]]/[[CCAR2]] regulatory interaction in Caenorhabditis elegans, and in utilizing this model organism to observe the effects of modulating sirtuin activity on the HSR, longevity, and proteostasis. The HSR is highly conserved in C. elegans and is mediated by the [[HSF1]] homolog, HSF-1. We have uncovered that negative regulation of the HSR by [[CCAR2]] is conserved in C. elegans and is mediated by the [[CCAR2]] ortholog, CCAR-1. This negative regulation requires the [[SIRT1]] homolog SIR-2.1. In addition, knockdown of CCAR-1 via ccar-1 RNAi works through SIR-2.1 to enhance stress resistance, motility, longevity, and proteostasis. This work therefore highlights the benefits of enhancing sirtuin activity to promote the HSR at the level of the whole organism.
|mesh-terms=* Acetylation
* Animals
* Caenorhabditis elegans
* Caenorhabditis elegans Proteins
* Disease Models, Animal
* Heat-Shock Response
* Huntington Disease
* Longevity
* Peptides
* Promoter Regions, Genetic
* Protein Binding
* RNA Interference
* RNA, Messenger
* Sirtuins
* Stress, Physiological
* Temperature
* Transcription Factors
|keywords=*  C. elegans 
* CCAR-1
* HSF-1
* SIR-2.1
* heat-shock response
* longevity
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156500
}}