c-Jun N-terminal kinases (JNKs) phosphorylate and augment transcriptional activity of c-Jun. JNKs originate from three genes that yield ten isoforms through alternative mRNA splicing, including JNK1α1,JNK1β1, JNK2α1, JNK2β1 and JNK3α1, which represent the p46 isoforms, and JNK1α2, JNK1β2, JNK2α2, JNK2β2 and JNK3β2, which represent the p54 isoforms. JNKs coordinate cell responses to stress and influence regulation of cell growth and ransformation. The human JNK1 (PRKM8, SAPK1, MAPK8) gene maps to chromosome 10q11.22 and shares 83% amino acid identity with JNK2. JNK1 is necessary for normal activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. Capsaicin activates JNK1 and p38 in Ras-transformed human breast epithelial cells. Nitrogen oxides (NOx) upregulate JNK1 in addition to c-Fos, c-Jun and other signaling kinases, including MEKK1 and p38.
Immunogen Information
Immunogen
KLH conjugated Synthetic peptide corresponding to human JNK1
Swissprot
Q91Y86,Q9WTU6,Q61831
Synonyms
MAPK8JNK1PRKM8SAPK1SAPK1CMitogen-activated protein kinase 8MAP kinase 8MAPK 8JNK-46Stress-activated protein kinase 1cSAPK1cStress-activated protein kinase JNK1c-Jun N-terminal kinase 1MAPK9JNK2PRKM9SAPK1AMi
Applications
Reactivity
Mouse,Rat
Tested Applications
IHC
Conjugation
Unconjugated
Dilution
IHC 1:200-1:500
Concentration
400 μg/mL
Storage Buffer
PBS with 0.02% sodium azide, 1% BSA and 50% glycerol, pH7.4