Редактирование: FLNA (раздел)

==Publications==

{{medline-entry
|title=[[SQSTM1]]/p62 mediates crosstalk between autophagy and the UPS in DNA repair.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27391408
|abstract=[[SQSTM1]]/p62 (sequestosome 1) selectively targets polyubiquitinated proteins for degradation via macroautophagy and the proteasome. Additionally, [[SQSTM1]] shuttles between the cytoplasmic and nuclear compartments, although its role in the nucleus is relatively unknown. Here, we report that [[SQSTM1]] dynamically associates with DNA damage foci (DDF) and regulates DNA repair. Upon induction of DNA damage [[SQSTM1]] interacts with [[FLNA]] (filamin A), which has previously been shown to recruit DNA repair protein [[RAD51]] ([[RAD51]] recombinase) to double-strand breaks and facilitate homologous recombination ([[HR]]). [[SQSTM1]] promotes proteasomal degradation of [[FLNA]] and [[RAD51]] within the nucleus, resulting in reduced levels of nuclear [[RAD51]] and slower DNA repair. [[SQSTM1]] regulates the ratio between [[HR]] and nonhomologous end joining (NHEJ) by promoting the latter at the expense of the former. This [[SQSTM1]]-dependent mechanism mediates the effect of macroautophagy on DNA repair. Moreover, nuclear localization of [[SQSTM1]] and its association with DDF increase with aging and are prevented by life-span-extending dietary restriction, suggesting that an imbalance in the mechanism identified here may contribute to aging and age-related diseases.
|mesh-terms=* Animals
* Autophagy
* Cell Nucleus
* DNA Damage
* DNA Repair
* Filamins
* Kinetics
* Mice, Inbred C57BL
* Models, Biological
* Proteasome Endopeptidase Complex
* Protein Transport
* Proteolysis
* Rad51 Recombinase
* Sequestosome-1 Protein
* Ubiquitin
|keywords=* DNA damage
* SQSTM1
* aging
* autophagy
* homologous recombination
* nonhomologous end joining
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391493
}}