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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 29 Mar 2014.

Mitogen-activated protein kinase kinase kinase 5

ASK1, apoptosis signal-regulating kinase 1, Dbf4
Mitogen-activated protein kinase (MAPK) signaling cascades include MAPK or extracellular signal-regulated kinase (ERK), MAPK kinase (MKK or MEK), and MAPK kinase kinase (MAPKKK or MEKK). MAPKK kinase/MEKK phosphorylates and activates its downstream protein kinase, MAPK kinase/MEK, which in turn activates MAPK. The kinases of these signaling cascades are highly conserved, and homologs exist in yeast, Drosophila, and mammalian cells. MAPKKK5 contains 1,374 amino acids with all 11 kinase subdomains. Northern blot analysis shows that MAPKKK5 transcript is abundantly expressed in human heart and pancreas. The MAPKKK5 protein phosphorylates and activates MKK4 (aliases SERK1, MAPKK4) in vitro, and activates c-Jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) during transient expression in COS and 293 cells; MAPKKK5 does not activate MAPK/ERK. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: JNK, p38, AP-1, V1a, MAPK
Papers using ASK1 antibodies
Regulation of the Subcellular Localization of Tumor Necrosis Factor Receptor–associated Factor (TRAF)2 by TRAF1 Reveals Mechanisms of TRAF2 Signaling
Choi Yongwon et al., In The Journal of Experimental Medicine, 1998
... ), JNK1 (N-19), MEKK1 (C-22), and ASK1 (H-300) were from Santa Cruz Biotechnology, Inc.; β-actin (Ab-1) was ...
Identification of a novel antiapoptotic protein that antagonizes ASK1 and CAD activities
Choi Eui-Ju et al., In The Journal of Cell Biology, 1994
... Rabbit anti-ASK1 and anti-hexahistidine (His) pAbs were purchased from Santa Cruz Biotechnology.
Papers on ASK1
Mcm10 deficiency causes defective-replisome-induced mutagenesis and a dependency on error-free postreplicative repair.
Bielinsky et al., Minneapolis, United States. In Cell Cycle, 27 Apr 2014
Replication gaps in mcm10-1 were likely caused by elongation defects, such as dbf4-1 mutants, which are compromised for origin activation did not display any hallmarks of replication stress.
Apoptosis signal-regulating kinase 1 as a therapeutic target.
Naguro et al., Tokyo, Japan. In Expert Opin Ther Targets, 24 Apr 2014
Apoptosis signal-regulating kinase 1 (ASK1) is one of the stress-responsive MAP3Ks.
Neuroprotective effect of muscone on glutamate-induced apoptosis in PC12 cells via antioxidant and Ca(2+) antagonism.
Liu et al., Hefei, China. In Neurochem Int, 14 Apr 2014
In conclusion, our results provided novel evidence that muscone protected PC12 cells against glutamate-induced apoptosis by attenuating ROS generation and Ca(2+) influx, via NR1 and CaMKII-depended ASK-1/JNK/p38 signaling pathways.
Effect of chemical modification on the ability of pyrrolidinium fullerene to induce apoptosis of cells transformed by JAK2 V617F mutant.
Kasahara et al., Tokyo, Japan. In Int Immunopharmacol, 12 Apr 2014
We previously reported that pyrrolidinium fullerene markedly induced the apoptosis of JAK2 V617F mutant-induced transformed cells through the reduction of apoptosis signal-regulating kinase 1 (ASK1), following inhibition of the c-Jun N-terminal kinase (JNK) pathway.
Ferulic acid attenuates the cerebral ischemic injury-induced decrease in peroxiredoxin-2 and thioredoxin expression.
Koh et al., Chinju, South Korea. In Neurosci Lett, 26 Mar 2014
Moreover, immunoprecipitation analysis showed that the interaction between thioredoxin and apoptosis signal-regulating kinase 1 (ASK1) decreased during MCAO, whereas ferulic acid prevented the MCAO-induced decrease in this interaction.
Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis.
Sil et al., Calcutta, India. In Arch Toxicol, Jul 2013
Emphasis has been given on the redox-sensitive ASK1 signalosome and its downstream JNK pathway.
Thioredoxin and thioredoxin target proteins: from molecular mechanisms to functional significance.
Lee et al., Cambridge, United States. In Antioxid Redox Signal, May 2013
The latter are extensively discussed, as ongoing research unveils more and more details about the complex signaling networks of Trx-sensitive signaling molecules such as apoptosis signal-regulating kinase 1, Trx interacting protein, and phosphatase and tensin homolog, thus highlighting the potential direct and indirect impact of their redox-dependent interaction with Trx.
Activation mechanisms of ASK1 in response to various stresses and its significance in intracellular signaling.
Ichijo et al., Tokyo, Japan. In Adv Biol Regul, 2013
Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase kinase kinase family.
Thioredoxin system in cell death progression.
Holmgren et al., Stockholm, Sweden. In Antioxid Redox Signal, 2013
The reduced/dithiol form of Trxs binds to apoptosis signal-regulating kinase 1 (ASK1) and inhibits its activity to prevent stress- and cytokine-induced apoptosis.
ASK1 promotes apoptosis of normal and malignant plasma cells.
Lin et al., Taipei, Taiwan. In Blood, 2012
A novel mechanism underlying the regulation of survival in normal and malignant plasma cells by ASK1.
Microspherule protein 2 associates with ASK1 and acts as a negative regulator of stress-induced ASK1 activation.
Zhao et al., Shanghai, China. In Febs Lett, 2012
MCRS2 plays a negative role in stress-induced ASK1 activation.
S100 proteins modulate protein phosphatase 5 function: a link between CA2+ signal transduction and protein dephosphorylation.
Kobayashi et al., Japan. In J Biol Chem, 2012
S100A1 and permanently active S100P inhibited the apoptosis signal-regulating kinase 1 (ASK1) and PP5 interaction, resulting the inhibition of dephosphorylation of phospho-ASK1 by PP5
TGF-β-activated kinase 1 (TAK1) and apoptosis signal-regulating kinase 1 (ASK1) interact with the promyogenic receptor Cdo to promote myogenic differentiation via activation of p38MAPK pathway.
Kang et al., Suwŏn, South Korea. In J Biol Chem, 2012
ASK1 and TAK1 function as MAP3 kinases in Cdo-mediated p38MAPK activation to promote myogenic differentiation.
A novel chromone derivative with anti-inflammatory property via inhibition of ROS-dependent activation of TRAF6-ASK1-p38 pathway.
Xu et al., Nanjing, China. In Plos One, 2011
Results indicate that the anti-inflammatory properties of DCO-6 was through inhibition of reactive oxygen species-dependent activation of TRAF6-ASK1-p38 pathway.
Therapeutic targets in the ASK1-dependent stress signaling pathways.
Ichijo et al., Tokyo, Japan. In Proc Jpn Acad Ser B Phys Biol Sci, 2011
Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase kinase kinase (MAP3K) family that activates downstream MAP kinases (MAPKs), c-Jun N-terminal kinases (JNKs) and p38 MAPKs, in response to various stresses, such as reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, lipopolysaccharide, and calcium overload.
Damage-induced phosphorylation of Sld3 is important to block late origin firing.
Toczyski et al., San Francisco, United States. In Nature, 2010
Here we show that the replication initiation protein Sld3 is phosphorylated by Rad53, and that this phosphorylation, along with phosphorylation of the Cdc7 kinase regulatory subunit Dbf4, blocks late origin firing in Saccharomyces cerevisiae.
A TNF- and c-Cbl-dependent FLIP(S)-degradation pathway and its function in Mycobacterium tuberculosis-induced macrophage apoptosis.
Basu et al., Calcutta, India. In Nat Immunol, 2009
TNF activated a pathway involving the kinases ASK1, p38 and c-Abl.
Apoptosis signal-regulating kinase 1 in stress and immune response.
Ichijo et al., Tokyo, Japan. In Annu Rev Pharmacol Toxicol, 2007
discusses the molecular mechanisms by which ASK1 functions in stress and immune responses and discuss the possible involvement of ASK1 in human diseases [review]
Mechanism of auxin perception by the TIR1 ubiquitin ligase.
Zheng et al., Seattle, United States. In Nature, 2007
Here we present the crystal structures of the Arabidopsis TIR1-ASK1 complex, free and in complexes with three different auxin compounds and an Aux/IAA substrate peptide.
ROS-dependent activation of the TRAF6-ASK1-p38 pathway is selectively required for TLR4-mediated innate immunity.
Ichijo et al., Tokyo, Japan. In Nat Immunol, 2005
complex of the adaptor molecule TRAF6 and ASK1 and subsequent activation of the ASK1-p38 pathway
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