Редактирование: SOCS1

Suppressor of cytokine signaling 1 (SOCS-1) (JAK-binding protein) (JAB) (STAT-induced STAT inhibitor 1) (SSI-1) (Tec-interacting protein 3) (TIP-3) [SSI1] [TIP3]

==Publications==

{{medline-entry
|title=Individual and combined effects of salinity and lipopolysaccharides on the immune response of juvenile Takifugu fasciatus.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30656452
|abstract=Lipopolysaccharides (LPS) and salinity are important variables in aquatic environments. High concentration of LPS and large changes in salinity seriously threat the survival of a variety of organisms, including fish. To reveal the effects of salinity and LPS on a fish immune response, we measured the immune-related parameters (total leukocyte count, total serum protein, albumin and globulin concentrations, complement [[C3]] concentration, and lysozyme activity) and genes (the expressions of [[TNF]]-α, IL-1β, and [[SOCS1]]-3 at the mRNA and protein levels) of juvenile Takifugu fasciatus exposed to phosphate buffered saline (PBS) or LPS (25 μg mL ) under different salinities (0, 15, and 30 ppt) for 24 h. Changes in key immunological indicators suggested that the LPS challenge induced considerable damage to T. fasciatus, whereas an increase in salinity mitigated the harmful effects. Moreover, although the immune responses in blood and other selected tissues (gill and kidney) were suppressed with an increase in salinity, the increased response in liver in saltwater enabled T. fasciatus to conquer large salinity variation during migration. The appropriate addition of salts appeared to be a sensible strategy to mitigate LPS-induced toxicity in the aquaculture of T. fasciatus.
|mesh-terms=* Aging
* Albumins
* Animals
* Blood Proteins
* Complement C3
* Cytokines
* Environmental Exposure
* Gene Expression Regulation
* Gills
* Globulins
* Muramidase
* RNA, Messenger
* Salinity
* Salt Tolerance
* Takifugu
* Water
|keywords=* Immune response
* Lipopolysaccharides
* Salinity
* Takifugu fasciatus
|full-text-url=https://sci-hub.do/10.1007/s10695-018-0607-9
}}
{{medline-entry
|title=[[SOCS1]] regulates senescence and ferroptosis by modulating the expression of p53 target genes.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29081404
|abstract=The mechanism by which p53 suppresses tumorigenesis remains poorly understood. In the context of aberrant activation of the JAK/STAT5 pathway, [[SOCS1]] is required for p53 activation and the regulation of cellular senescence. In order to identify p53 target genes acting during the senescence response to oncogenic [[STAT5A]], we characterized the transcriptome of [[STAT5A]]-expressing cells after [[SOCS1]] inhibition. We identified a set of [[SOCS1]]-dependent p53 target genes that include several secreted proteins and genes regulating oxidative metabolism and ferroptosis. Exogenous [[SOCS1]] was sufficient to regulate the expression of p53 target genes and sensitized cells to ferroptosis. This effect correlated with the ability of [[SOCS1]] to reduce the expression of the cystine transporter [[SLC7A11]] and the levels of glutathione. [[SOCS1]] and [[SOCS1]]-dependent p53 target genes were induced during the senescence response to oncogenic [[STAT5A]], RasV12 or the tumor suppressor [[PML]]. However, while [[SOCS1]] sensitized cells to ferroptosis neither RasV12 nor [[STAT5A]] mimicked the effect. Intriguingly, [[PML]] turned cells highly resistant to ferroptosis. The results indicate different susceptibilities to ferroptosis in senescent cells depending on the trigger and suggest the possibility of killing senescent cells by inhibiting pathways that mediate ferroptosis resistance.
|mesh-terms=* Cell Line
* Cell Line, Tumor
* Cellular Senescence
* Gene Expression Regulation
* Humans
* Suppressor of Cytokine Signaling 1 Protein
* Tumor Suppressor Protein p53
|keywords=* KAP1
* ferroptosis
* senescence
* suppressor of cytokine signaling
* tumor suppressor
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5680560
}}
{{medline-entry
|title=Daily Socs1 rhythms alter with aging differentially in peripheral clocks in male Wistar rats: therapeutic effects of melatonin.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28331994
|abstract=Suprachiasmatic nucleus (SCN) in synchronization with the peripheral clocks regulates the temporal oscillations leading to overt rhythms. Aging leads to attenuation of such circadian regulation, accompanied by increased inflammatory mediators prevalently the cytokines. Suppressors of cytokine signaling (SOCS) family of proteins such as SOCS 1, 3 and cytokine-inducible SH2-containing protein (CIS) negatively regulate the cytokine signaling pathway. The role of [[SOCS1]] in aging and circadian system is obscure. We therefore studied the daily rhythms of rSocs1 mRNA expression at Zeitgeber time (ZT) -0, 6, 12 and 18 in peripheral clocks such as liver, kidney, intestine and heart of 3, 12 and 24 months (m) old male Wistar rats. Interestingly the peripheral clocks studied displayed a rhythmic rSocs1 gene expression in 3 months. In 12 months group, 12 h phase advance in liver and 12 h phase delay in kidney and heart was observed with abolition of rhythms in intestine. Aging (24 months group) resulted in a phase advance by 6 h in liver and heart with abolition of rhythms in intestine in 24 months group. Kidney was also significantly affected upon aging with significant decrease in the rSocs1 levels and abolition of rhythms. The decrease in melatonin levels with aging is associated with decreased immunity and increased oxidative stress. The exogenous administration of melatonin has been linked to play a role in re-synchronization of circadian rhythms, reducing oxidative stress and enhancing immune properties. We therefore had studied the effect of exogenous melatonin upon age induced changes in daily rSocs1 gene expression patterns. Melatonin treatment partially restored the rhythms and daily pulse (ratio of maximum:minimum levels) in liver and intestine in 12 months group. Melatonin administration resulted in a significant increase in mean 24 h rSocs1 expression in intestine and heart of 24 months group compared to that of 3 months. The melatonin administration resulted in differential restoration of rSocs1 rhythms and levels in various tissues of 24 months old group. The sensitivity of 24 months old animals to melatonin found in the present study is a step towards endorsing melatonin as an important anti-aging therapeutic drug.
|mesh-terms=* Aging
* Animals
* Biological Clocks
* Kidney
* Liver
* Male
* Melatonin
* Myocardium
* RNA, Messenger
* Rats
* Rats, Wistar
* Suppressor of Cytokine Signaling 1 Protein
|keywords=* Aging
* Circadian rhythms
* Melatonin
* Peripheral clocks
* Socs1
|full-text-url=https://sci-hub.do/10.1007/s10522-017-9687-7
}}
{{medline-entry
|title=Differential response to intrahippocampal interleukin-4/interleukin-13 in aged and exercise mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27916728
|abstract=Normal aging is associated with low-grade neuroinflammation that results from age-related priming of microglial cells. Further, aging alters the response to several anti-inflammatory factors, including interleukin (IL)-4 and IL-13. One intervention that has been shown to modulate microglia activation in the aged brain, both basally and following an immune challenge, is exercise. However, whether engaging in exercise can improve responsiveness to anti-inflammatory cytokines is presently unknown. The current study evaluated whether prior exercise training increases sensitivity to anti-inflammatory cytokines that promote the M2 (alternative) microglia phenotype in adult (5-month-old) and aged (23-month-old) C57BL/6J mice. After 8weeks of exercise or control housing, mice received bilateral hippocampal injections of an IL-4/IL-13 cocktail or vehicle. Twenty-four hours later hippocampal samples were collected and analyzed for expression of genes associated with the M1 (inflammatory) and M2 microglia phenotypes. Results show that IL-4/IL-13 administration increased expression of the M2-associated genes found in inflammatory zone 1 (Fizz1), chitinase-like 3 (Ym1), Arginase-1 (Arg1), [[SOCS1]], IL-1ra, and CD206. In response to IL-4/IL-13 administration, aged mice showed increased hippocampal expression of the M2-related genes Arg1, [[SOCS1]], Ym1, and CD206 relative to adult mice. Aged mice also showed increased expression of IL-1β relative to adults, which was unaffected by wheel running or IL-4/IL-13. Wheel running was found to have modest effects on expression of Ym1 and Fizz1 in aged and adult mice. Collectively, our findings indicate that aged mice show a differential response to anti-inflammatory cytokines relative to adult mice and that exercise has limited effects on modulating this response.
|mesh-terms=* Aging
* Animals
* Arginase
* Gene Expression
* Hippocampus
* Immunologic Factors
* Intercellular Signaling Peptides and Proteins
* Interleukin-13
* Interleukin-4
* Lectins
* Lectins, C-Type
* Male
* Mannose-Binding Lectins
* Mice, Inbred C57BL
* Microglia
* Motor Activity
* Receptors, Cell Surface
* Receptors, Interleukin-1
* Suppressor of Cytokine Signaling 1 Protein
* beta-N-Acetylhexosaminidases
|keywords=* IL-1ra
* M2
* anti-inflammatory
* cytokine
* microglia
* wheel running
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5800496
}}
{{medline-entry
|title=Aging diminishes the resistance of AO rats to EAE: putative role of enhanced generation of GM-CSF Expressing CD4  T cells in aged rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26448779
|abstract=Aging influences immune response and susceptibility to EAE in a strain specific manner. The study was designed to examine influence of aging on EAE induction in Albino Oxford (AO) rats. Differently from 3-month-old (young) rats, which were resistant to EAE induction, the majority of aged (24-26-month-old) rats developed mild chronic form of EAE. On 16(th) day post-immunization, when in aged rats the neurological deficit reached plateau, more mononuclear cells, including CD4  T lymphocytes was retrieved from spinal cord of aged than young rats. The frequencies of IL-17  and GM-CSF  cells within spinal cord infiltrating CD4  lymphocytes were greater in aged rats. To their increased frequency contributed the expansion of GM-CSF   IL-17   IFN-γ  cells, which are highly pathogenic in mice. The expression of the cytokines (IL-1β and IL-23/p19) driving GM-CSF   IL-17   IFN-γ   cell differentiation in mice was also augmented in aged rat spinal cord mononuclear cells. Additionally, in aged rat spinal cord the expansion of GM-CSF   IL-17-IFN-γ- CD4  T lymphocytes was found. Consistently, the expression of mRNAs for IL-3, the cytokine exhibiting the same expression pattern as GM-CSF, and IL-7, the cytokine driving differentiation of GM-CSF   IL-17-IFN-γ- CD4   lymphocytes in mice, was upregulated in aged rat spinal cord mononuclear cells, and the tissue, respectively. This was in accordance with the enhanced generation of the brain antigen-specific GM-CSF  CD4  lymphocytes in aged rat draining lymph nodes, as suggested by (i) the higher frequency of GM-CSF  cells (reflecting the expansion of IL-17-IFN-γ- cells) within their CD4  lymphocytes and (ii) the upregulated GM-CSF and IL-3 mRNA expression in fresh CD4  lymphocytes and [[MBP]]-stimulated draining lymph node cells and IL-7 mRNA in lymph node tissue from aged rats. In agreement with the upregulated GM-CSF expression in aged rats, strikingly more CD11b   CD45(int) (activated microglia) and CD45(hi) (mainly proinflammatory dendritic cells and macrophages) cells was retrieved from aged than young rat spinal cord. Besides, expression of mRNA for [[SOCS1]], a negative regulator of proinflammatory cytokine expression in innate immunity cells, was downregulated in aged rat spinal cord mononuclear cells. The study revealed that aging may overcome genetic resistance to EAE, and indicated the cellular and molecular mechanisms contributing to this phenomenon in AO rats.

|keywords=* AO rats
* Aging
* EAE
* GM-CSF
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4596406
}}