Редактирование: NSMCE2 (раздел)

==Publications==

{{medline-entry
|title=[[NSMCE2]] suppresses cancer and aging in mice independently of its SUMO ligase activity.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26443207
|abstract=The SMC5/6 complex is the least understood of SMC complexes. In yeast, smc5/6 mutants phenocopy mutations in sgs1, the [[BLM]] ortholog that is deficient in Bloom's syndrome (BS). We here show that [[NSMCE2]] (Mms21, in Saccharomyces cerevisiae), an essential SUMO ligase of the SMC5/6 complex, suppresses cancer and aging in mice. Surprisingly, a mutation that compromises [[NSMCE2]]-dependent SUMOylation does not have a detectable impact on murine lifespan. In contrast, [[NSMCE2]] deletion in adult mice leads to pathologies resembling those found in patients of BS. Moreover, and whereas [[NSMCE2]] deletion does not have a detectable impact on DNA replication, [[NSMCE2]]-deficient cells also present the cellular hallmarks of BS such as increased recombination rates and an accumulation of micronuclei. Despite the similarities, [[NSMCE2]] and [[BLM]] foci do not colocalize and concomitant deletion of Blm and Nsmce2 in B lymphocytes further increases recombination rates and is synthetic lethal due to severe chromosome mis-segregation. Our work reveals that SUMO- and [[BLM]]-independent activities of [[NSMCE2]] limit recombination and facilitate segregation; functions of the SMC5/6 complex that are necessary to prevent cancer and aging in mice. 
|mesh-terms=* Aging
* Animals
* B-Lymphocytes
* Base Sequence
* Cells, Cultured
* Chromosome Segregation
* DNA Breaks, Double-Stranded
* DNA Mutational Analysis
* DNA Replication
* Female
* Haploinsufficiency
* Humans
* Ligases
* Mice, 129 Strain
* Mice, Inbred C57BL
* Mice, Knockout
* Neoplasms
* Protein Transport
* RecQ Helicases
* Sumoylation
* Tumor Suppressor Proteins
* Ubiquitin-Protein Ligases
|keywords=* NSMCE2
* SMC5/6
* SUMO
* chromosome segregation
* mouse models
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4641528
}}