Редактирование: SESN2 (раздел)

==Publications==

{{medline-entry
|title=Copy Number Alterations in Papillary Thyroid Carcinomas: Does Loss of [i][[SESN2]][/i] Have a Role in Age-related Different Prognoses?
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/32859642
|abstract=Thyroid cancer is the only tumor in which age is an important prognostic factor. In papillary thyroid carcinomas (PTC), 45 years of age seems to be a key point that divides adult patients into two groups, with different clinical features. The aim of the study was to perform a microarray-based analysis in two groups of patients (<45 and ≥45 years old), in order to verify the occurrence of specific copy number alterations (CNAs) that could be associated to different patient behaviors associated with age. In order to search and compare genomic alterations that may be related to age, we evaluated the occurrence of CNAs in the genome of 24 PTC samples, divided in two groups (<45 and ≥45 years old). We identified only one region showing a statistically significant difference between the groups (p=0.00357): a deletion of approximately 537 kps in 1p35.3., which was more frequent in patients aged 45 years or older. This is the region where, among others, the gene [[SESN2]] is located, which is activated under oxidative stress and plays an antioxidant role, in addition to protecting the genetic material from damage generated by reactive oxygen species (ROS). This is the first time that a CNA involving the deletion of the [[SESN2]] gene is associated with papillary thyroid carcinomas, particularly in patients aged 45 years and older, indicating that this deletion would lead to a more malignant and prominent tumoral behavior associated to a worst prognosis.

|keywords=* Papillary thyroid cancer
* SESN2
* aCGH
* deletion
* senescence
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7472442
}}
{{medline-entry
|title=Loss of sestrin 2 potentiates the early onset of age-related sensory cell degeneration in the cochlea.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28818524
|abstract=Sestrin 2 ([[SESN2]]) is a stress-inducible protein that protects tissues from oxidative stress and delays the aging process. However, its role in maintaining the functional and structural integrity of the cochlea is largely unknown. Here, we report the expression of [[SESN2]] protein in the sensory epithelium, particularly in hair cells. Using C57BL/6J mice, a mouse model of age-related cochlear degeneration, we observed a significant age-related reduction in [[SESN2]] expression in cochlear tissues that was associated with early onset hearing loss and accelerated age-related sensory cell degeneration that progressed from the base toward the apex of the cochlea. Hair cell death occurred by caspase-8 mediated apoptosis. Compared to C57BL/6J control mice, Sesn2 KO mice displayed enhanced expression of proinflammatory genes and activation of basilar membrane macrophages, suggesting that loss of [[SESN2]] function provokes the immune response. Together, these results suggest that Sesn2 plays an important role in cochlear homeostasis and immune responses to stress.
|mesh-terms=* Aging
* Animals
* Basilar Membrane
* Cellular Senescence
* Cochlea
* Hair Cells, Auditory
* Hearing Loss
* Macrophages
* Mice, Knockout
* Nuclear Proteins
* Peroxidases
|keywords=* age-related hearing loss
* cochlea
* inflammation
* macrophages
* outer hair cells
* sestrin 2 (SESN2)
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5605466
}}