J2455
JNK1, active, GST tagged from mouse
PRECISIO® Kinase, recombinant, expressed in baculovirus infected Sf9 cells, ≥90% (SDS-PAGE), buffered aqueous glycerol solution
Synonym(s):
JNK, JNK1A1, JNK21B1/2, PRKM8, SAPK1
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About This Item
UNSPSC Code:
12352200
NACRES:
NA.32
recombinant
expressed in baculovirus infected Sf9 cells
Quality Level
product line
PRECISIO® Kinase
Assay
≥90% (SDS-PAGE)
form
buffered aqueous glycerol solution
specific activity
92-124 nmol/min·mg
mol wt
~71 kDa
UniProt accession no.
shipped in
dry ice
storage temp.
−70°C
Gene Information
mouse ... Mapk8(26419)
Biochem/physiol Actions
As a member of the MAP kinase family, JNK1 is known to play a role in the induction of apoptosis through various stimuli such as TNFa.JNK1 also is influences cell migration via phosphorylation of paxillin.JNK1 is also a crucial mediator of obesity and insulin resistance and a potential target for therapeutics.
JNK1 (c-Jun N-terminal kinase 1) is a member of the MAPK (mitogen activated protein kinase) family that controls gene expression by phosphorylation of transcription factors. It is linked with apoptosis, brain development and learning ability. JNK1 also influences cell migration via phosphorylation of paxillin. JNK1 also regulates obesity and insulin resistance.
Physical form
Supplied in 50 mM Tris-HCl, pH 7.5, with 150 mM NaCl, 0.2 5mM DTT, 0.1 mM EGTA, 0.1 mM EDTA, 0.1 mM PMSF, and 25% glycerol.
Legal Information
PRECISIO is a registered trademark of Merck KGaA, Darmstadt, Germany
Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
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Hélène Henrie et al.
The Journal of cell biology, 219(7) (2020-06-04)
The stress-induced c-Jun N-terminal kinase (JNK) controls microtubule dynamics by enhancing both microtubule growth and rescues. Here, we show that upon cell stress, JNK directly phosphorylates the microtubule rescue factor CLIP-170 in its microtubule-binding domain to increase its rescue-promoting activity.
Cai Huang et al.
Nature, 424(6945), 219-223 (2003-07-11)
The c-Jun amino-terminal kinase (JNK) is generally thought to be involved in inflammation, proliferation and apoptosis. Accordingly, its substrates are transcription factors and anti-apoptotic proteins. However, JNK has also been shown to be required for Drosophila dorsal closure, and MAP
C Tournier et al.
Science (New York, N.Y.), 288(5467), 870-874 (2000-05-08)
The c-Jun NH2-terminal kinase (JNK) is activated when cells are exposed to ultraviolet (UV) radiation. However, the functional consequence of JNK activation in UV-irradiated cells has not been established. It is shown here that JNK is required for UV-induced apoptosis
Prescott T Leach et al.
Neurobiology of learning and memory, 118, 162-166 (2014-12-30)
Increased training often results in stronger memories but the neural changes responsible for these stronger memories are poorly understood. It is proposed here that higher levels of training that result in stronger memories recruit additional cell signaling cascades. This study
Jiro Hirosumi et al.
Nature, 420(6913), 333-336 (2002-11-26)
Obesity is closely associated with insulin resistance and establishes the leading risk factor for type 2 diabetes mellitus, yet the molecular mechanisms of this association are poorly understood. The c-Jun amino-terminal kinases (JNKs) can interfere with insulin action in cultured
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