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anti-Rat (Rattus) RPS6KA2 Antikörper:
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Human Monoclonal RPS6KA2 Primary Antibody für IF, IHC (p) - ABIN562719
Passariello, Gayanilo, Kritzer, Thakur, Cozacov, Rusconi, Wieczorek, Sanders, Li, Kapiloff: p90 ribosomal S6 kinase 3 contributes to cardiac insufficiency in ?-tropomyosin Glu180Gly transgenic mice. in American journal of physiology. Heart and circulatory physiology 2013
Human Monoclonal RPS6KA2 Primary Antibody für WB - ABIN534385
Fisher, Blenis: Evidence for two catalytically active kinase domains in pp90rsk. in Molecular and cellular biology 1996
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Human Monoclonal RPS6KA2 Primary Antibody für ELISA, WB - ABIN532714
Frödin, Gammeltoft: Role and regulation of 90 kDa ribosomal S6 kinase (RSK) in signal transduction. in Molecular and cellular endocrinology 1999
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Data suggest that millisecond dynamic changes in PDZ1 domain conformation are responsible for higher affinity of scribble PDZ1 for phosphorylated ligands; oligopeptide fragments of RPS6KA2 and MCC were used as ligands in these nuclear magnetic resonance chemical shift experiments. (RPS6KA2 = ribosomal protein S6 kinase 2; MCC = mutated in colorectal cancer protein)
RSK1 and 3 but not RSK2 are down-regulated in breast tumour and are associated with disease progression. RSK may be a key component in the progression and metastasis of breast cancer.
Data indicate that S6 kinase 2 (S6K2) can phosphorylate histone H3 at position Thr45, which may play a role during cell proliferation and/or differentiation.
Kinome screening revealed RPS6KA2 expression, in human pancreatic cancer cells, protects against erlotinib induced apoptosis.
genetic association study in Han population in China: Data suggest that SNPs in RSK3 (rs2229712) and in MEK1 (rs28730804) demonstrate gene-gene interaction that affects antidepressant drug outcome in female patients with major depressive disorder.
Overexpression of RSK3 or RSK4 supports tumor cell proliferation upon PI3K inhibition both in vitro and in vivo therby contributing to drug resistance.
p90RSK2 is dispensable for BCR-ABL-induced myeloid leukemia, but may be required for pathogenesis and lineage determination in FLT3-internal tandem duplication-induced hematopoietic transformation.
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.
Characterization of the terminal domain as a protein kinase
chronic activation CREB and p90RSK in the epileptic hippocampus may be closely associated with the histopathological changes of Ammon's horn sclerosis
overexpressed in breast tumors
The accumulation of S6K2 in the nuclei of cancer cells and the correlation with the expression of PCNA and Ki-67 suggest the involvement of S6K2 in the regulation of malignant growth
p90Rsk-mediated modulation of Hdm2 nuclear is linked to cytoplasmic shuttling with the diminished ability of p53 to regulate cell cycle checkpoints that ultimately leads to transformation
The large C-terminal domain of ERK5 is not required for binding or activation of RSK by ERK5.
The above results suggest that RPS6KA2 is a putative tumour suppressor gene to explain allele loss at 6q27.
there is a functional link between S6K1 II and CK2 signaling, which involves the regulation of S6K1 II nuclear export by CK2-mediated phosphorylation of Ser-17
We confirmed that Raf1(L613V) knock-in confers a NS-like phenotype, including cardiac hypertrophy. Active RSK3 was increased in Raf1(L613V) mice. Constitutive RSK3 gene deletion prevented the Raf1(L613V)-dependent concentric growth in width of the cardiac myocyte and attenuated cardiac hypertrophy in female mice.
RSK3 is required for the induction of interstitial cardiac fibrosis in alpha-tropomyosin Glu180Gly transgenic mice.
Anchored RSK3 transduces signals that modulate pathologic myocyte growth in cardiac hypertrophy.
p90RSK2 is dispensable for BCR-Abl-induced myeloid leukemia, but may be required for pathogenesis and lineage determination in Flt3-internal tandem duplication-induced hematopoietic transformation.
activation and translocation of p90 ribosomal S6 protein kinase requires RANTES-mediated chemokine transcription in astrocytes
p90Rsk2 and Emi1 functionally interact during oocyte maturation
inhibition of p90RSK prevented H2O2-mediated cTnI (Ser(23/24)) phosphorylation but not ERK1/2 and PKCalpha/betaII activation
p90RSK is a novel regulator of cardiac NHE1 activity by phosphorylating NHE1 serine 703 and a new pathological mediator of I/R injury in the heart
RSK2 is a key regulator for cell transformation induced by tumor promoters such as EGF and TPA.
These data indicate that Ribosomal s6 kinase 2 negatively regulates axon elongation via the MAPK pathway.
This gene encodes a member of the RSK (ribosomal S6 kinase) family of serine/threonine kinases. This kinase contains 2 non-identical kinase catalytic domains and phosphorylates various substrates, including members of the mitogen-activated kinase (MAPK) signalling pathway. The activity of this protein has been implicated in controlling cell growth and differentiation. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
ribosomal protein S6 kinase alpha-2
, ribosomal protein S6 kinase, 90kD, polypeptide 2
, 90 kDa ribosomal protein S6 kinase 2
, MAP kinase-activated protein kinase 1c
, MAPK-activated protein kinase 1c
, MAPKAP kinase 1c
, p90-RSK 2
, ribosomal S6 kinase 3
, ribosomal protein S6 kinase alpha 2
, S6K-alpha 2
, protein-tyrosine kinase Mpk-9