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JNKJun N-terminal Kinase
JNKJunk (File Name Extension)
JNKJun Nuclear Kinase
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References in periodicals archive ?
Harmful effects of these pathways could be reduced by turning down JNK or TGF-beta activity.
Extracellular regulated kinase (ERK) 1/2 (MAPK1/3), P38 (MAPK14), c-Jun N-terminal kinase (JNK) (MAPK8), and ERK5 (MAPK7) are four components of MAPK pathways.[13] On activation, MAPKs phosphorylate and activate an array of transcription factors that regulate many important physiological and pathological processes in the cell including growth and differentiation, stress, adaptation to the environment, and the inflammatory response.[14],[15],[16],[17]
The membranes were incubated with primary antibodies against cyclinD1 (ab134175), p21 (ab109199), cytochrome C (ab90529), B cell lymphoma-2 (Bcl-2, ab196495), Bcl-2-associated X protein (Bax, ab182733), cleaved caspase-3 (ab2302), cleaved caspase-9 (ab2324), matrix metalloproteinase (MMP)-2 (ab97779), MMP-9 (ab137867), vimentin (ab137321), c-Jun (ab32137), phospho (p)-c-Jun (ab32385), [beta]-actin (ab8229, all Abcam, Cambridge, UK), c-Jun N-terminal protein kinase (JNK; 9252), or p-JNK (9251, both Cell Signaling Technology, USA) at 4[degrees]C overnight.
The acquisition will also offer JNK clients access to all of Uphold's crypto to fiat trading pairs and assets, introducing Uphold's platform to a new group of institutional investors.
There are three major subfamilies in the MAPK: extracellular signal-regulated kinase (Erk), p38 and c-Jun-N terminal kinase (JNK).16
The antibodies for PPAR[alpha], JNK, p-JNK, TRAF2, Bax, Bcl-2, LC3, Beclin 1, and caspase-3 were provided by Proteintech (Chicago, IL, USA).
Membranes were probed with rabbit polyclonal antibodies against phosphorylated p38 MAPK, total p38 MAPK, phosphorylated JNK and total JNK, rabbit monoclonal antibodies against phosphorylated c-Jun and total c-Jun, or mouse monoclonal antibody against [beta]-actin.
Cells were seeded into six well plates and divided into four groups: control group, agonist-CD137 group, JNK inhibition group, and DMSO group.
These findings strongly indicate that the prevention of fluctuating hyperglycemia is essential to reduce macrophage activation and JNK inhibition may be a potential therapeutic method to inhibit macrophage activation and the resulting inflammatory response.
JNK phosphorylates numerous important substrates, including transcription factors AP-1, c-Jun, and Fos, leading to activation of nuclear response [3-5].