Редактирование: STAG3 (раздел)

==Publications==

{{medline-entry
|title=Dynamics of cohesin proteins [[REC8]], [[STAG3]], SMC1 beta and [[SMC3]] are consistent with a role in sister chromatid cohesion during meiosis in human oocytes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/20634189
|abstract=Sister chromatid cohesion is essential for ordered chromosome segregation at mitosis and meiosis. This is carried out by cohesin complexes, comprising four proteins, which seem to form a ring-like complex. Data from animal models suggest that loss of sister chromatid cohesion may be involved in age-related non-disjunction in human oocytes. Here, we describe the distribution of cohesins throughout meiosis in human oocytes. We used immunofluorescence in human oocytes at different meiotic stages to detect cohesin subunits [[REC8]], [[STAG3]], SMC1 beta and [[SMC3]], [also synaptonemal complex (SC) protein 3 and shugoshin 1]. Samples from euploid fetuses and adult women were collected, and 51 metaphase I (MI) and 113 metaphase II (MII) oocytes analyzed. SMC1 beta transcript levels were quantified in 85 maturing germinal vesicle (GV) oocytes from 34 women aged 19-43 years by real-time PCR. At prophase I, cohesin subunits [[REC8]], [[STAG3]], SMC1 beta and [[SMC3]] overlapped with the lateral element of the SC. Short cohesin fibers are observed in the oocyte nucleus during dictyate arrest. All four subunits are observed at centromeres and along chromosomal arms, except at chiasmata, at MI and are present at centromeric domains from anaphase I to MII. SMC1 beta transcripts were detected (with high inter-sample variability) in GV oocytes but no correlation between SMC1 beta mRNA levels and age was found. The dynamics of cohesins [[REC8]], [[STAG3]], SMC1 beta and [[SMC3]] suggest their participation in sister chromatid cohesion throughout the whole meiotic process in human oocytes. Our data do not support the view that decreased levels of SMC1 beta gene expression in older women are involved in age-related non-disjunction.
|mesh-terms=* Adult
* Aging
* Cell Cycle Proteins
* Cell Nucleus
* Centromere
* Chondroitin Sulfate Proteoglycans
* Chromatids
* Chromosomal Proteins, Non-Histone
* Chromosome Aberrations
* DNA-Binding Proteins
* Female
* Fetus
* Humans
* Meiosis
* Nuclear Proteins
* Oocytes
* RNA, Messenger
* Synaptonemal Complex
* Young Adult

|full-text-url=https://sci-hub.do/10.1093/humrep/deq180
}}
{{medline-entry
|title=Defective cohesin is associated with age-dependent misaligned chromosomes in oocytes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/18252055
|abstract=Aneuploidy often results from chromosome misalignment at metaphases. Oocytes from senescence-accelerated mice (SAM) exhibit increased chromosome misalignment with age, which originates from nuclear factors. This work sought to further characterize the underlying defects of chromosome misalignments. Using immunofluorescence microscopy with specific antibodies, several specific components associated with spindles or chromosomes, including centrosomes, centromeres and cohesin complex were examined. No obvious differences were found in the distribution of centrosome focus at the spindle pole of oocytes from young and aged SAM, regardless of chromosome alignments, although cytoplasmic centrosome foci were significantly reduced in aged SAM (P < 0.0001). Oocytes from both young and aged SAM exhibited centromere-associated protein-E (CENP-E) at centromeres of all chromosomes, including misaligned chromosomes from aged SAM, demonstrating that CENP-E did not contribute to chromosome misalignments. Notably, both meiotic cohesin proteins located between sister chromatids, [[REC8]] (recombinant 8), [[STAG3]] (stromal antigen 3) and SMC1beta, were remarkably reduced in oocytes from aged SAM. Further, degradation of the cohesin was even more obvious in SAM than in hybrid F1 mice with age, which may explain why SAM are vulnerable to aneuploidy. This natural ageing mouse model shows that defective cohesin coincides with increased incidence of chromosome misalignment and precocious separations of sister chromatids.
|mesh-terms=* Aging
* Aneuploidy
* Animals
* Cell Cycle Proteins
* Cells, Cultured
* Centromere
* Chromosomal Instability
* Chromosomal Proteins, Non-Histone
* Chromosome Segregation
* Female
* Kinetochores
* Mice
* Nuclear Proteins
* Oocytes
* Phosphoproteins

|full-text-url=https://sci-hub.do/10.1016/s1472-6483(10)60562-7
}}