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Antikörper

Phospho-Ask1 (Ser83) (Clone: G4) rabbit mAb

Produktgrößen
20 µl
£631,00
12-4075-20UL
200 µl
£1021,00
12-4075-200UL
Über dieses Produkt
SKU:
12-4075
Zusätzliche Namen:
Apoptosis signal-regulating kinase 1; Mitogen-activated protein kinase kinase kinase 5; MAPK/ERK kinase kinase 5; MAP3K5; MAPKKK5; MEKK5
translate.label.attr.clone:
Ask1S83-G4
Klonalität:
Monoclonal
Konjugat:
Unconjugated
Weitere Details:
Stress signaling in cells are partly mediated through c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). A kinase upstream of these stress-mediated pathways is apoptosis signal-regulating kinase 1 (ASK1). ASK1 is a serine/threonine kinase that belongs to the family of mitogen-activated protein kinase kinase kinase (MAP3K). It is endogenously expressed in various cells. Various stress signaling activates ASK1 including reactive oxygen species (ROS); tumor necrosis factor alpha (TNFa); lipopolysaccharide (LPS) and endoplasmic reticulum (ER) stress. These events ultimately lead to the activation of JNK and p38 MAPK. As a result; ASK1-MAPK signaling is associated with various cellular stress responses including apoptosis; differentiation; and inflammation. Several studies show that aberrant ASK1 signaling leads to severe human diseases such as neurodegenerative diseases; induction of inflammatory diseases and cancer. The phosphorylation of the threonine residues 838 (Thr838) in human and Thr845 in mice is important for ASK1 activation. At basal inactive state; ASK1 is a homooligomer; which binds to another ASK1 via its C-terminal coiled-coil domain. The N-terminal coiled-coil of ASK1 binds to thioredoxin (Trx); which suppresses ASK1 kinase activity. Under oxidative stress; oxidized Trx is separated from ASK1 and unbond ASK1 is activated by phosphorylation. Calcium influx and oxidative stress can elicit phosphorylation of the ASK1. After H2O2 injury; tumor necrosis factor 2; (TRAF2) and TRAF6 act as positive regulator of ASK1. 14-3-3 proteins; act as negative regulator of ASK1 by binding to the C-terminal of ASK1 after Ser966 phosphorylation. However oxidative stress promotes dephosphorylation of Ser966 and lead to detachment of 14-3-3. TNF and Fas death receptor activate ASK1. ASK1 is an early signal stress responder to oxidative stress in cerebral ischemia. ASK1 has also been implicated in thrombosis; brain edema; inflammatory response; and reactive gliosis.
Format:
Purified
Host:
Rabbit
Immunogen:
A synthetic phospho-peptide corresponding to residues surrounding Ser83 of human phospho Ask1
Isotyp:
Rabbit IgG1k
Reaktivitäten:
Human, Mouse, Rat
Versandbedingungen:
Blue Ice
Lagerbedingungen:
Store at -20[o]C. Avoid repeated freeze and thaw cycles.
Hersteller:
Abeomics
Typ:
Antibodies:Monoclonal Antibody
  • Datenblatt des Herstellers:1.jpg
Fig 2 : Western blot analysis of C6 cell extract treated with imatinib or treated with PV using Phospho-Ask1 (Ser83) antibody at 0.01 µg/mL. Ask1S83-G4.
Fig-3: Peptide blocking flow cytometric analysis of C6 cells secondary antibody only negative control (light blue) or imatinib-treated (red) or pervandadate-treated (green) or imatinib and blocked with phospho-peptide (black) or pervanadate and blocked with phospho peptide (gold) or imatinib and blocked with non-phospho peptide (dark blue) or pervanadate and blocked with non-phospho peptide (purple) using Phospho-Ask1 (Ser83) antibody Ask1S83-G4 at 1ng/mL.
Fig-4: Western blot analysis of L929 cell extract treated with 20% FBS using Phospho-Ask1 (Ser83) antibody Ask1S83-G4 at 0.01µg/mL.
Fig-4: Western blot analysis of L929 cell extract treated with 20% FBS using Phospho-Ask1 (Ser83) antibody Ask1S83-G4 at 0.01µg/mL.
Fig-5: Flow cytometric analysis of K562 cells secondary antibody only negative control (blue) or treated with imatinib (red) or with IFNa + IL-4 + pervanadate (green) using Phospho-Ask1 (Ser83) antibody Ask1S83-G4 at 5ng/mL.