J4644
Anti-phospho-JNK1/2 (pThr183/pTyr185) antibody produced in rabbit
affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-phospho-SAPK (pTpY183/185), Anti-phospho-Stress Activated Protein Kinase (pTpY183/185), Anti-phospho-c-Jun N-terminal Kinase 1/2 (pTpY183/185)
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous glycerol solution
species reactivity
rat, human
technique(s)
immunocytochemistry: 1:250
immunofluorescence: 1:250
immunohistochemistry: Assay Dependent
western blot: 1:200-1:2000 (using human 293 cells treated with UV radiation)
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
Gene Information
human ... MAPK8(5599)
General description
c-Jun N-terminal kinase (JNK, SAPK) is an extensively studied memebr of the MAPK family of kinases and is critical in mediating the apoptotic signaling. There are three isoforms of JNK, JNK 1, 2 and 3. JNK 1 and 2 are ubiquitously expressed; JNK 3 is restricted to cardiac and neuronal tissues.
Immunogen
synthetic peptide derived from a region of JNK1 & 2 that contains threonine183 and tyrosine185.
Application
Anti-phospho-JNK1/2 (pThr183/pTyr185 ) antibody concentration is formulated to be used at the recommended dilutions by application.
Biochem/physiol Actions
JNK (c-Jun N-terminal kinase) is phosphorylated by MAPK (mitogen activated protein kinase) kinases 4 and 7 at Thr183 and Tyr185, leading to its activation. It is however not clear as to which MAPKK phosphorylates which amino acid residue. The activation of JNK is highly regulated and is in response to the stress signals that the cell faces. JNK phosphorylates c-Jun, the most important member of the AP-1 transcription factor family that is involved in survival, apoptosis, proliferation and tumorigenesis. JNK also activates other transcription factors such as c-myc and p53. JNK is involved in the phosphorylation of proteins such as Bad, Bcl2 and Bim that result in the execution of apoptosis by release of cytochrome c from mitochondria.
Anti-phospho-JNK1/2 (SAPK) (pThr183/pTyr185 ) specifically recognizes the endogenous, active forms of JNK1 and 2 phosphorylated at threonine 183 and tyrosine 185.
Anti-phospho-JNK1/2 (SAPK) (pThr183/pTyr185 ) specifically recognizes the endogenous, active forms of JNK1 and 2 phosphorylated at threonine 183 and tyrosine 185.
Physical form
Solution in Dulbecco′s phosphate buffered saline (without Mg2+ and Ca2+), pH 7.3, with 50% glycerol, 1% bovine serum albumin (BSA) (IgG and preservatives free) and 0.05% sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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recommended
Storage Class Code
10 - Combustible liquids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Gaurav Verma et al.
Journal of cellular physiology, 227(5), 1791-1795 (2011-07-07)
Apoptosis or programmed cell death is an extremely coordinated phenomenon that involves the participation of a complex interacting crosstalk between the endoplasmic reticulum and mitochondria. This involves a series of signaling molecules like stress kinases, caspases, Bcl-2 family of proteins
Ksenya Cohen-Katsenelson et al.
The Biochemical journal, 439(3), 381-390 (2011-07-14)
JNK (c-Jun N-terminal kinase) is part of a MAPK (mitogen-activated protein kinase) signalling cascade. Scaffold proteins simultaneously associate with various components of the MAPK signalling pathway and play a crucial role in signal transmission and MAPK regulation. WDR62 (WD repeat
F Urano et al.
Science (New York, N.Y.), 287(5453), 664-666 (2000-01-29)
Malfolded proteins in the endoplasmic reticulum (ER) induce cellular stress and activate c-Jun amino-terminal kinases (JNKs or SAPKs). Mammalian homologs of yeast IRE1, which activate chaperone genes in response to ER stress, also activated JNK, and IRE1alpha-/- fibroblasts were impaired
Anning Lin et al.
Aging cell, 1(2), 112-116 (2003-07-29)
Age-associated changes in apoptotic rates have been observed in a number of different tissues. While the implications of these findings remain unclear, a better understanding of how apoptosis is regulated may further our understanding of the aging process. The role
Jing Liu et al.
Cell research, 15(1), 36-42 (2005-02-03)
JNK is a key regulator of many cellular events, including programmed cell death (apoptosis). In the absence of NF-kB activation, prolonged JNK activation contributes to TNF-a induced apoptosis. JNK is also essential for UV induced apoptosis. However, recent studies reveal
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