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MSK1 was overexpressed in 148 out of 329 colorectal cancer (CRC) patients. CRC patients with high MSK1 expression had shorter overall survival than those with low MSK1, especially among patients with stage III tumors. Overexpression of MSK1 is associated with poor prognosis in CRC and is connected to tumor aggressiveness.
High MSK1 is associated with improved breast cancer-specific survival in early stage invasive breast cancer patients, and has additional prognostic value in HER2-negative and non-basal like disease.
Our findings indicate that MSK1/beta-catenin signaling serves as an escape survival signal upon PI3K inhibition and provides a strong rationale for the combined use of PI3K and MSK1/beta-catenin inhibition to induce lethal growth inhibition in human GBM cells.
Results show that MSK1 phosphorylates H3S10 through p38-MAPK pathway in gastric cancer patients.
Interrupting MSK1 activation is a new target for antioxidants.
Increased MSK1 activity is critically important for Epstein-Barr virus LMP1-promoted cell proliferation and transformation.
KSHV activates the MSK1/2-CREB1 pathway during primary infection and that it depends on this pathway for viral lytic replication. I
Authors conclude that paramyxoviruses trigger the DNA damage response, a pathway required for MSK1 activation of phospho Ser 276 RelA formation to trigger the IRF7-RIG-I amplification loop necessary for mucosal interferon production.
These results highlight the relevance of MSK1 in the up-regulation of RARbeta by prostaglandin E2.
Data suggest that MSK1 and MSK2 are the major CREB kinases in fibroblast-like synoviocytes from rheumatoid arthritis patients stimulated with lysophosphatidic acid and that phosphorylation of CREB1 at Ser-133 plays a significant role in IL-8 production.
MSK1 plays an important role for hormone-dependent breast cancer growth
MSK1 and MSK2 are required for maximal TFF 1 induction.
Angiopoietin 2-mediated signaling via survivin/ref-1/MSK-1 pathway promotes doxorubicin resistance in HepG2 cells.
Astaxanthin attenuates the UVB-induced secretion of prostaglandin E2 and interleukin-8 in human keratinocytes by interrupting MSK1 phosphorylation in a ROS depletion-independent manner
MSK1 is an important downstream kinase involved in CS-induced NF-kappaB activation
MSK1 is a direct and potent transcriptional activator when targeted to c-fos promotor, and when targeted to alpha-globin promoter induces H3 S28 phosphorylation reactivating expression of this polycomb-silenced gene.
MSK1- and MSK2-mediated H3K27me3S28 phosphorylation serves as a mechanism to activate a subset of PcG target genes determined by the biological stimuli and thereby modulate the gene expression program determining cell fate.
In this study, by applying a novel method, we have identified the phosphorylation sites in human MSK1 mitogen- and stress-activated protein kinase 1, and show that MRK-beta could also activate MSK1 through direct interaction.
MiR-148a attenuates paclitaxel resistance of hormone-refractory, drug-resistant prostate cancer PC3 cells by regulating MSK1 expression
Bile acid regulates MUC2 transcription in colon cancer cells via positive EGFR/PKC/Ras/ERK/CREB, PI3K/Akt/IkappaB/NF-kappaB and p38/MSK1/CREB pathways and negative JNK/c-Jun/AP-1 pathway.
essential role of the C-terminal domain of MSK1 for its constitutive interaction with group V secretory phospholipase A(2), which appears essential to support VEGF-mediated PAF synthesis
These data suggest that the kinase activity of MSK1 is not directly required for several forms of synaptic plasticity or spatial learning and memory.
These data of this study provided important new insights into the mechanism by which the MAPK/MSK1 signaling cassette confers neuroprotection against excitotoxic insults.
Data suggest that expression of Rps6ka5 in gonadotroph cell line is up-regulated by GnRH signaling and is required for Cga expression; GnRH-activates Rps6ka5 targets at the first nucleosome just downstream from the transcriptional start site. (Rps6ka5= mitogen and stress-activated protein kinase 1; GnRH = gonadotropin-releasing hormone; Cga = gonadotropin alpha subunit)
chromatin modifier, MSK1/2, has a role in suppressing endocrine and promoting acinar differentiation during pancreatic development
abnormal regulation of MSK1 contributes to the development of L-DOPA-induced dyskinesia and to the concomitant increase in striatal FosB, which may occur via increased histone H3 phosphorylation at the fosB promoter
Accelerated apoptotic death and in vivo turnover of erythrocytes have been found in mice lacking functional MSK1/MSK2.
Results suggest that MSK1/2 plays a significant role in the regulation of ischemia-induced progenitor cell proliferation and neurogenesis
MSK1 has a role in malignant transformation and skin cancer development, but is inhibited by chrysin derivative 69407
the impact of MSK1 on glucocorticoid receptor-mediated transactivation
MSK1 is an important novel molecule involved in RANKL signaling and osteoclast differentiation
MSK1/2 knockout results in reduced IL-10 secretion.
MSK1-deficient mice exhibit a decreased capacity to entrain to a new light cycle, attenuated Period1 expression, histone phosporylation and CREB phosphorylation.
these data reveal that MSK1 serves as a critical regulator of hippocampal physiology and function
data reveal a critical role for MSK1/2 as regulators of both basal and activity-dependent progenitor cell proliferation and morphological maturation in the subgranular zone
This study demonstrated that MSK1 is an integral part of a signaling pathway that underlies the adaptive response to synaptic and environmental experience.
by suppression of both NF-kappaB and ERK1/2-MSK1 signaling, DMF inhibits maturation of DCs and subsequently Th1 and Th17 cell differentiation.
the signaling pathways of MAPK, MSK1, and NF-kappaB play important roles in thrombin-induced iNOS expression in alveolar macrophages
Comparison of the effects of SB-747651A, both in vitro and in cells, demonstrated that SB-747651A exhibited improved selectivity over H89 and Ro 31-8220 and therefore represents a useful tool to study MSK function in cells.
phosphorylation was required for up-regulation of the EMI2 activity in the oocytes. These results suggest that mouse MSK1 may play a key role in the metaphase-II arrest through phosphorylation of EMI2
Serine/threonine-protein kinase that is required for the mitogen or stress-induced phosphorylation of the transcription factors CREB1 and ATF1 and for the regulation of the transcription factors RELA, STAT3 and ETV1/ER81, and that contributes to gene activation by histone phosphorylation and functions in the regulation of inflammatory genes. Phosphorylates CREB1 and ATF1 in response to mitogenic or stress stimuli such as UV-C irradiation, epidermal growth factor (EGF) and anisomycin. Plays an essential role in the control of RELA transcriptional activity in response to TNF and upon glucocorticoid, associates in the cytoplasm with the glucocorticoid receptor NR3C1 and contributes to RELA inhibition and repression of inflammatory gene expression. In skeletal myoblasts is required for phosphorylation of RELA at 'Ser-276' during oxidative stress. In erythropoietin-stimulated cells, is necessary for the 'Ser-727' phosphorylation of STAT3 and regulation of its transcriptional potential. Phosphorylates ETV1/ER81 at 'Ser-191' and 'Ser-216', and thereby regulates its ability to stimulate transcription, which may be important during development and breast tumor formation. Directly represses transcription via phosphorylation of 'Ser-1' of histone H2A. Phosphorylates 'Ser-10' of histone H3 in response to mitogenics, stress stimuli and EGF, which results in the transcriptional activation of several immediate early genes, including proto- oncogenes c-fos/FOS and c-jun/JUN. May also phosphorylate 'Ser-28' of histone H3. Mediates the mitogen- and stress-induced phosphorylation of high mobility group protein 1 (HMGN1/HMG14). In lipopolysaccharide-stimulated primary macrophages, acts downstream of the Toll-like receptor TLR4 to limit the production of pro- inflammatory cytokines. Functions probably by inducing transcription of the MAP kinase phosphatase DUSP1 and the anti- inflammatory cytokine interleukin 10 (IL10), via CREB1 and ATF1 transcription factors. Plays a role in neuronal cell death by mediating the downstream effects of excitotoxic injury.
90 kDa ribosomal protein S6 kinase 5
, RSK-like protein kinase
, nuclear mitogen- and stress-activated protein kinase 1
, ribosomal protein S6 kinase alpha-5
, mitogen- and stress-activated protein kinase-1
, ribosomal protein S6 kinase, polypeptide 5
, mitogen and stress-activated protein kinase 1
, ribosomal protein S6 kinase, 90kDa, polypeptide 5