HCSGD entry for RPS6KB1
1. General information
| Official gene symbol | RPS6KB1 |
|---|---|
| Entrez ID | 6198 |
| Gene full name | ribosomal protein S6 kinase, 70kDa, polypeptide 1 |
| Other gene symbols | PS6K S6K S6K-beta-1 S6K1 STK14A p70 S6KA p70(S6K)-alpha p70-S6K p70-alpha |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000082 | G1/S transition of mitotic cell cycle | IMP | biological_process |
| GO:0003009 | Skeletal muscle contraction | IEA | biological_process |
| GO:0004672 | Protein kinase activity | IDA IEA | molecular_function |
| GO:0004674 | Protein serine/threonine kinase activity | IEA | molecular_function |
| GO:0004711 | Ribosomal protein S6 kinase activity | IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005524 | ATP binding | IEA | molecular_function |
| GO:0005634 | Nucleus | IDA IEA | cellular_component |
| GO:0005737 | Cytoplasm | IDA | cellular_component |
| GO:0005739 | Mitochondrion | IDA IEA | cellular_component |
| GO:0005741 | Mitochondrial outer membrane | IEA | cellular_component |
| GO:0005829 | Cytosol | TAS | cellular_component |
| GO:0005840 | Ribosome | IEA | cellular_component |
| GO:0006468 | Protein phosphorylation | IDA | biological_process |
| GO:0006915 | Apoptotic process | IEA | biological_process |
| GO:0007165 | Signal transduction | IEA TAS | biological_process |
| GO:0007281 | Germ cell development | IEA | biological_process |
| GO:0007568 | Aging | IEA | biological_process |
| GO:0007584 | Response to nutrient | IEA | biological_process |
| GO:0007616 | Long-term memory | IEA | biological_process |
| GO:0008152 | Metabolic process | IDA | biological_process |
| GO:0008286 | Insulin receptor signaling pathway | TAS | biological_process |
| GO:0009408 | Response to heat | IEA | biological_process |
| GO:0009611 | Response to wounding | IEA | biological_process |
| GO:0009612 | Response to mechanical stimulus | IEA | biological_process |
| GO:0009636 | Response to toxic substance | IEA | biological_process |
| GO:0009749 | Response to glucose | IEA | biological_process |
| GO:0009986 | Cell surface | IEA | cellular_component |
| GO:0014732 | Skeletal muscle atrophy | IEA | biological_process |
| GO:0014878 | Response to electrical stimulus involved in regulation of muscle adaptation | IEA | biological_process |
| GO:0014911 | Positive regulation of smooth muscle cell migration | IEA | biological_process |
| GO:0016310 | Phosphorylation | IDA | biological_process |
| GO:0016477 | Cell migration | IEA | biological_process |
| GO:0030054 | Cell junction | IEA | cellular_component |
| GO:0031929 | TOR signaling | IDA | biological_process |
| GO:0032496 | Response to lipopolysaccharide | IEA | biological_process |
| GO:0032868 | Response to insulin | IEA | biological_process |
| GO:0032870 | Cellular response to hormone stimulus | IEA | biological_process |
| GO:0033574 | Response to testosterone | IEA | biological_process |
| GO:0033762 | Response to glucagon | IEA | biological_process |
| GO:0034612 | Response to tumor necrosis factor | IEA | biological_process |
| GO:0042277 | Peptide binding | IEA | molecular_function |
| GO:0042493 | Response to drug | IEA | biological_process |
| GO:0043005 | Neuron projection | IEA | cellular_component |
| GO:0043066 | Negative regulation of apoptotic process | IMP | biological_process |
| GO:0043201 | Response to leucine | IEA | biological_process |
| GO:0043491 | Protein kinase B signaling | IEA | biological_process |
| GO:0045202 | Synapse | IEA | cellular_component |
| GO:0045471 | Response to ethanol | IEA | biological_process |
| GO:0045727 | Positive regulation of translation | IMP | biological_process |
| GO:0045931 | Positive regulation of mitotic cell cycle | IMP | biological_process |
| GO:0045948 | Positive regulation of translational initiation | IMP | biological_process |
| GO:0046324 | Regulation of glucose import | IEA | biological_process |
| GO:0046627 | Negative regulation of insulin receptor signaling pathway | IEA IMP | biological_process |
| GO:0048015 | Phosphatidylinositol-mediated signaling | TAS | biological_process |
| GO:0048471 | Perinuclear region of cytoplasm | IEA | cellular_component |
| GO:0048633 | Positive regulation of skeletal muscle tissue growth | IEA | biological_process |
| GO:0048661 | Positive regulation of smooth muscle cell proliferation | IEA | biological_process |
| GO:0051384 | Response to glucocorticoid | IEA | biological_process |
| GO:0071363 | Cellular response to growth factor stimulus | IDA | biological_process |
| GO:2001237 | Negative regulation of extrinsic apoptotic signaling pathway | IEA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.2258313362 | 0.4323143536 | 0.9070243973 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.1748162004 |
| GSE13712_SHEAR | Up | 0.4253767166 |
| GSE13712_STATIC | Up | 0.7005216377 |
| GSE19018 | Down | -0.2399936472 |
| GSE19899_A1 | Up | 0.2348666459 |
| GSE19899_A2 | Up | 0.2941713928 |
| PubMed_21979375_A1 | Down | -0.6406769945 |
| PubMed_21979375_A2 | Up | 0.4358057384 |
| GSE35957 | Down | -0.2380434745 |
| GSE36640 | Down | -0.2175684850 |
| GSE54402 | Up | 0.2165365807 |
| GSE9593 | Down | -0.0912462259 |
| GSE43922 | Down | -0.0308516742 |
| GSE24585 | Up | 0.4524335726 |
| GSE37065 | Up | 0.1084980940 |
| GSE28863_A1 | Up | 0.0185348519 |
| GSE28863_A2 | Down | -0.2693499023 |
| GSE28863_A3 | Down | -0.1539435892 |
| GSE28863_A4 | Down | -0.0635517210 |
| GSE48662 | Up | 0.0966139488 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-215-5p | MIMAT0000272 | MIRT024333 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-192-5p | MIMAT0000222 | MIRT026123 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-103a-3p | MIMAT0000101 | MIRT027002 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-98-5p | MIMAT0000096 | MIRT027419 | Microarray | Functional MTI (Weak) | 19088304 |
| hsa-miR-16-5p | MIMAT0000069 | MIRT031441 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-877-3p | MIMAT0004950 | MIRT037006 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-877-5p | MIMAT0004949 | MIRT037328 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 21 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26977878 | Consequently, dual inhibition of EGFR/HER2 and CDK4/6 invokes a more potent suppression of TSC2 phosphorylation and hence mTORC1/S6K/S6RP activity |
| 25785348 | Pathway analysis revealed that the OIS-induced ubiquitinome alterations mainly affected 3 signaling networks: eIF2 signaling, eIF4/p70S6K signaling, and mTOR signaling |
| 25635535 | Previous work showed that augmented arginase-II (Arg-II) and S6K1 interact with each other to promote endothelial senescence through uncoupling of endothelial nitric oxide synthase (eNOS) |
| 25635535 | Silencing Arg-II or p38a or S6K1 inhibits each other in senescence endothelial cells |
| 25587030 | Geroconversion was associated with active mTOR and S6 kinase (S6K) |
| 25587030 | Without affecting Akt phosphorylation, PMA increased phosphorylation of S6K (T389) and S6 (S240/244), and that was completely prevented by rapamycin |
| 25484082 | Using human nonsenescent "young" and replicative senescent endothelial cells as well as Apolipoprotein E-deficient (apoe(-/-)Arg2(+/+)) and Arg2-deficient apoe(-/-) (apoe(-/-)arg2(-/-)) mice fed a high-fat diet for 10 wk as the atherosclerotic animal model, we show here that overexpression of ARG2 in the young cells suppresses endothelial autophagy with concomitant enhanced expression of RICTOR, the essential component of the MTORC2 complex, leading to activation of the AKT-MTORC1-RPS6KB1/S6K1 (ribosomal protein S6 kinase, 70kDa, polypeptide 1) cascade and inhibition of PRKAA/AMPK (protein kinase, AMP-activated, alpha catalytic subunit) |
| 25484082 | Moreover, silencing RPS6KB1 or expression of a constitutively active PRKAA prevented autophagy suppression by ARG2 or H160F |
| 25484082 | In line with the above observations, genetic ablation of Arg2 in apoe(-/-) mice reduced RPS6KB1, enhanced PRKAA signaling and endothelial autophagy in aortas, which was associated with reduced atherosclerosis lesion formation |
| 25484082 | Taken together, the results demonstrate that ARG2 impairs endothelial autophagy independently of the L-arginine ureahydrolase activity through activation of RPS6KB1 and inhibition of PRKAA, which is implicated in atherogenesis |
| 25087910 | Autophagy in cells was examined by detecting for LC3, Beclin-1, m-TOR, and p70S6K, as well as by analyzing autophagosomes |
| 25087910 | Glucosamine could activate autophagy in a dose-dependent manner within 24 h and inhibit the phosphorylation of m-TOR and p70S6K |
| 25087910 | The percentage of SA-beta-Gal-positive cells induced by H2 O2 treatment was decreased by glucosamine, accompanied by the decline of p70S6K phosphorylation |
| 24860943 | Long term exposure to L-arginine accelerates endothelial cell senescence through arginase-II and S6K1 signaling |
| 24860943 | While acute L-arginine treatment enhances endothelial NO production accompanied with superoxide production and activation of S6K1 but no up-regulation of arginase-II, chronic L-arginine supplementation causes endothelial senescence, up-regulation of the adhesion molecule expression, and eNOS-uncoupling (decreased NO and enhanced superoxide production), which are associated with S6K1 activation and up-regulation of arginase-II |
| 24860943 | Silencing either S6K1 or arginase-II inhibits up-regulation/activation of each other, prevents endothelial dysfunction, adhesion molecule expression, and senescence under the chronic L-arginine supplementation condition |
| 24860943 | These results demonstrate that S6K1 and arginase-II form a positive circuit mediating the detrimental effects of chronic L-arginine supplementation on endothelial cells |
| 24677687 | Reviewed are also specific interactions between mTOR/S6K1 and ROS-DNA damage signaling pathways |
| 24677687 | While the primary target of each of these agents may be different the data obtained on several human cancer cell lines, WI-38 fibroblasts and normal lymphocytes suggest common downstream mechanism in which the decline in mTOR/S6K1 signaling and translation rate is coupled with a reduction of oxidative phosphorylation and ROS that leads to decreased oxidative DNA damage |
| 24036549 | Here we show that, while not affecting cyclin D1, siRNA for p70S6K partially prevented loss of RP (replicative/regenerative potential) during p21-induced cell cycle arrest |
| 24036549 | Thus S6K and MEK play different roles in geroconversion |
| 23832324 | In senescent VSMCs, Arg-II and S6K1, ERK-p66Shc, and p53 signaling levels were increased |
| 23832324 | Conversely, silencing p66Shc reduced ERK and S6K1 signaling and Arg-II levels and cell senescence/apoptosis |
| 23727633 | Levels of phosphorylated p70S6K did not decrease with glucocorticoid treatment indicating mTOR remained active |
| 23523798 | CKIIalpha knock-down or CKII inhibitor treatment strikingly increased phosphorylation of mTOR, p70S6K, an mTOR substrate, and AKT, whereas CKIIalpha overexpression reduced this phosphorylation event |
| 23363784 | Although the primary target of each on these agents may be different the data are consistent with the downstream mechanism in which the decline in mTOR/S6K signaling and translation rate is coupled with a decrease in oxidative phosphorylation, (revealed by DeltaPsim) that leads to reduction of ROS and oxidative DNA damage |
| 23296670 | The present chapter describes simple procedures to reliably evaluate the response of cultured cell to nutrients through the longevity protein p66(SHC1) and the mTOR/S6K cascade, which might be used to study cellular senescence and its chemical modulation by pharmaceutical agents in vitro |
| 23276696 | HMGA2 regulates the in vitro aging and proliferation of human umbilical cord blood-derived stromal cells through the mTOR/p70S6K signaling pathway |
| 22928666 | Positive crosstalk between arginase-II and S6K1 in vascular endothelial inflammation and aging |
| 22928666 | Augmented activities of both arginase and S6K1 are involved in endothelial dysfunction in aging |
| 22928666 | This study was to investigate whether or not there is a crosstalk between arginase and S6K1 in endothelial inflammation and aging in senescent human umbilical vein endothelial cells and in aging mouse models |
| 22928666 | Moreover, overexpressing S6K1 in nonsenescent cells increases, whereas silencing S6K1 in senescent cells decreases Arg-II gene expression/activity through regulation of Arg-II mRNA stability |
| 22928666 | Furthermore, S6K1 overexpression exerts the same effects as Arg-II on endothelial senescence and inflammation responses, which are prevented by silencing Arg-II, demonstrating a role of Arg-II as the mediator of S6K1-induced endothelial aging |
| 22928666 | Interestingly, mice that are deficient in Arg-II gene (Arg-II(-/-) ) are not only protected from age-associated increase in Arg-II, VCAM1/ICAM1, aging markers, and eNOS-uncoupling in the aortas but also reveal a decrease in S6K1 activity |
| 22928666 | Similarly, silencing Arg-II in senescent cells decreases S6K1 activity, demonstrating that Arg-II also stimulates S6K1 in aging |
| 22928666 | Our study reveals a novel mechanism of mutual positive regulation between S6K1 and Arg-II in endothelial inflammation and aging |
| 22928666 | Targeting S6K1 and/or Arg-II may decelerate vascular aging and age-associated cardiovascular disease development |
| 22442749 | The downstream target of mTORC1, the kinase S6K1, induces insulin resistance by phosphorylation of insulin receptor substrate-1, thereby increasing the metabolic burden of beta-cells |
| 22160218 | In terms of molecular mechanism, knockdown of DEPDC6/DEPTOR expression in HuH-7 cells caused S6K and 4E-BP activation, but suppressed Akt |
| 21544240 | Mammalian target of rapamycin (mTOR)/S6K1 signalling emerges as a critical regulator of aging |
| 21544240 | Yet, a role of mTOR/S6K1 in aging-associated vascular endothelial dysfunction remains unknown |
| 21544240 | In this study, we investigated the role of S6K1 in aging-associated endothelial dysfunction and effects of the polyphenol resveratrol on S6K1 in aging endothelial cells |
| 21544240 | We show here that senescent endothelial cells displayed higher S6K1 activity, increased superoxide production and decreased bioactive nitric oxide (NO) levels than young endothelial cells, which is contributed by eNOS uncoupling |
| 21544240 | Silencing S6K1 in senescent cells reduced superoxide generation and enhanced NO production |
| 21544240 | Conversely, over-expression of a constitutively active S6K1 mutant in young endothelial cells mimicked endothelial dysfunction of the senescent cells through eNOS uncoupling and induced premature cellular senescence |
| 21544240 | Like the mTOR/S6K1 inhibitor rapamycin, resveratrol inhibited S6K1 signalling, resulting in decreased superoxide generation and enhanced NO levels in the senescent cells |
| 21544240 | Consistent with the data from cultured cells, an enhanced S6K1 activity, increased superoxide generation, and decreased bioactive NO levels associated with eNOS uncoupling were also detected in aortas of old WKY rats (aged 20-24 months) as compared to the young animals (1-3 months) |
| 21544240 | Treatment of aortas of old rats with resveratrol or rapamycin inhibited S6K1 activity, oxidative stress, and improved endothelial NO production |
| 21544240 | Our data demonstrate a causal role of the hyperactive S6K1 in eNOS uncoupling leading to endothelial dysfunction and vascular aging |
| 21544240 | Resveratrol improves endothelial function in aging, at least in part, through inhibition of S6K1 |
| 21544240 | Targeting S6K1 may thus represent a novel therapeutic approach for aging-associated vascular disease |
| 18320031 | SIRT1 overexpression antagonizes cellular senescence with activated ERK/S6k1 signaling in human diploid fibroblasts |
| 18320031 | Our data also exposed that overexpression of SIRT1 was accompanied by enhanced activation of ERK and S6K1 signaling |
| 18320031 | It was also observed that the expression of SIRT1 and phosphorylation of ERK and S6K1 was declined in senescent 2BS |
| 18320031 | These findings suggested that SIRT1-promoted cell proliferation and antagonized cellular senescence in human diploid fibroblasts may be, in part, via the activation of ERK/ S6K1 signaling |
| 16600555 | By use of conditioned medium, we found a growth promoting impact of fibroblasts compared with control medium from epithelial cells associated with activation of ERK1/2, Akt, p70S6K, and EGF receptor |
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