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Ribosomal protein S6 kinase, 70kDa, polypeptide 2

This gene encodes a member of the RSK (ribosomal S6 kinase) family of serine/threonine kinases. This kinase contains 2 nonidentical kinase catalytic domains and phosphorylates the S6 ribosomal protein and eucaryotic translation initiation factor 4B (eIF4B). Phosphorylation of S6 leads to an increase in protein synthesis and cell proliferation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: p70S6K, mTOR, Akt, CAN, p70
Papers on S6K2
mTORC1 signaling and IL-17 expression: Defining pathways and possible therapeutic targets.
Yin et al., Changsha, China. In Eur J Immunol, Dec 2015
mTORC1 positively modulates IL-17 expression through several pathways, i.e STAT3, -HIF1α, -S6K1, and -S6K2.
The S6K protein family in health and disease.
Simabuco et al., Limeira, Brazil. In Life Sci, Jul 2015
Studies involving S6K2 are scarce.
S6 kinase signaling: tamoxifen response and prognostic indication in two breast cancer cohorts.
Stål et al., Stockholm, Sweden. In Endocr Relat Cancer, Jun 2015
We found that S6K1 correlated with proliferation, HER2 status, and cytoplasmic AKT activity, whereas high protein expression levels of S6K2 and phosphorylated (p) S6K were more common in ER-positive, and low-proliferative tumors with pAKT-s473 localized to the nucelus.
MicroRNA-193a-3p and -5p suppress the metastasis of human non-small-cell lung cancer by downregulating the ERBB4/PIK3R3/mTOR/S6K2 signaling pathway.
Yao et al., Shanghai, China. In Oncogene, Feb 2015
In addition, we discovered that ERBB4 and S6K2 were the direct targets of miR-193a-3p and that PIK3R3 and mTOR were the direct targets of miR-193a-5p in NSCLC.
Development of organometallic S6K1 inhibitors.
Marmorstein et al., Philadelphia, United States. In J Med Chem, Feb 2015
Biochemical data demonstrate that EM5 and FL772 inhibit the kinase with IC50 value in the low nanomolar range at 100 μM ATP and that the more potent FL772 compound has a greater than 100-fold specificity over S6K2.
Revealing Different Roles of the mTOR-Targets S6K1 and S6K2 in Breast Cancer by Expression Profiling and Structural Analysis.
Lundström et al., Linköping, Sweden. In Plos One, 2014
The mTORC1 downstream effectors S6K1, S6K2, and 4EBP1 are amplified and overexpressed in breast cancer, associated with a poor outcome and divergent endocrine treatment benefit.
Age-Related Neurodegeneration Prevention Through mTOR Inhibition: Potential Mechanisms and Remaining Questions.
Laberge et al., Novato, United States. In Curr Top Med Chem, 2014
We explore the small molecule alternatives to rapamycin and propose future directions for their development, mainly by exploring the possibility of targeting the downstream effectors of mTOR: S6K1 and especially S6K2.
hnRNPA1 couples nuclear export and translation of specific mRNAs downstream of FGF-2/S6K2 signalling.
Pardo et al., Ottawa, Canada. In Nucleic Acids Res, 2014
Fibroblast growth factor 2 (FGF-2) signalling-induced S6 kinase 2 (S6K2) activation is necessary, but the downstream mediator(s) coupling this kinase to the translational response is unknown.
Ghrelin-induced food intake and adiposity depend on central mTORC1/S6K1 signaling.
Castañeda et al., Potsdam, Germany. In Mol Cell Endocrinol, 2014
Chronic peripheral administration of ghrelin induced a significant increase in body weight, fat mass and food efficiency in wild-type and S6K2-knockout but not in S6K1-knockout mice.
mTORC1 targets the translational repressor 4E-BP2, but not S6 kinase 1/2, to regulate neural stem cell self-renewal in vivo.
Bordey et al., New Haven, United States. In Cell Rep, 2013
Although 4E-BP2 knockdown promoted NSC differentiation, p70 S6 kinase 1 and 2 (S6K1/S6K2) knockdown did not affect NSC differentiation but reduced NSC soma size and prevented hyperactive mTORC1-induced increase in soma size.
S6K2: The Neglected S6 Kinase Family Member.
Seckl et al., London, United Kingdom. In Front Oncol, 2012
S6 kinase 2 (S6K2) is a member of the AGC kinases super-family.
The mTOR effectors 4EBP1 and S6K2 are frequently coexpressed, and associated with a poor prognosis and endocrine resistance in breast cancer: a retrospective study including patients from the randomised Stockholm tamoxifen trials.
Stål et al., In Breast Cancer Res, 2012
INTRODUCTION: mTOR and its downstream effectors the 4E-binding protein 1 (4EBP1) and the p70 ribosomal S6 kinases (S6K1 and S6K2) are frequently upregulated in breast cancer, and assumed to be driving forces in tumourigenesis, in close connection with oestrogen receptor (ER) networks.
S6 kinase 2 deficiency enhances ketone body production and increases peroxisome proliferator-activated receptor alpha activity in the liver.
Um et al., Suwŏn, South Korea. In Hepatology, 2012
S6K2 regulates hepatic energy homeostasis by repressing PPARalpha activity.
Regulation and function of ribosomal protein S6 kinase (S6K) within mTOR signalling networks.
Fingar et al., Ann Arbor, United States. In Biochem J, 2012
mTORC1 (mammalian TORC1) phosphorylates and activates S6K1 and S6K2, whose first identified substrate was rpS6 (ribosomal protein S6), a component of the 40S ribosome.
Metabolic control by S6 kinases depends on dietary lipids.
Tschöp et al., Düsseldorf, Germany. In Plos One, 2011
metabolic functions of S6K in vivo play a key role as a molecular interface connecting dietary lipids to the endogenous control of energy metabolism.
Differential expression of S6K2 dictates tissue-specific requirement for S6K1 in mediating aberrant mTORC1 signaling and tumorigenesis.
Pandolfi et al., Boston, United States. In Cancer Res, 2011
S6K2 expression dictates tissue-specific requirement for S6K1 in mediating aberrant mTORC1 signaling and tumorigenesis
S6 kinase 2 promotes breast cancer cell survival via Akt.
Basu et al., Fort Worth, United States. In Cancer Res, 2011
Study shows that the two homologues of S6K have distinct effects on Akt activation and cell survivalin breast cancer.
Genetic variation in RPS6KA1, RPS6KA2, RPS6KB1, RPS6KB2, and PDK1 and risk of colon or rectal cancer.
Wolff et al., Salt Lake City, United States. In Mutat Res, 2011
Data show that genetic variation in RPS6KA1, RPS6KA2, and PRS6KB2 were associated with risk of developing colon cancer while only genetic variation in RPS6KA2 was associated with altering risk of rectal cancer.
Functions and regulation of the 70kDa ribosomal S6 kinases.
Gout et al., San Diego, United States. In Int J Biochem Cell Biol, 2011
Dysregulation of S6 kinases contributes to the pathogenesis of human diseases.
S6 kinase deletion suppresses muscle growth adaptations to nutrient availability by activating AMP kinase.
Pende et al., Paris, France. In Cell Metab, 2007
Energy stress and muscle cell atrophy are specifically triggered by the S6K1 deletion, independent of S6K2 activity.
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