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Documenti fondamentali

14-327-M

Sigma-Aldrich

JNK1α1/SAPK1c Protein, active, 10 µg

Active, recombinant full-length human JNK1α1/SAPK1c with an N-terminal His-tag, for use in Kinase Assays.

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About This Item

Codice UNSPSC:
12352202
eCl@ss:
32160405
NACRES:
NA.41

Origine biologica

human

Livello qualitativo

100

Ricombinante

expressed in Sf21 cells

Nome Commerciale

Upstate®

Attività specifica

(For Specific Activity data, refer to the Certificate of Analysis for individual lots of this enzyme.)

PM

Mw 45 kDa

Purificato mediante

(Ni2+/NTA-agarose)

Reattività contro le specie

human

Produttore/marchio commerciale

Upstate®

tecniche

activity assay: suitable (kinase)

Numero d’accesso

 (FUNCTION: SwissProt: P45983 # JNK1 isoforms display different binding patterns: beta-1 preferentially binds to c-Jun, whereas alpha-1, alpha-2, and beta- 2 have a similar low level of binding to both c-Jun or ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms. )
NM_002750.2

N° accesso NCBI

NM_002750.2
NM_139046.1
NM_139047.1
NM_139049.1

N° accesso UniProt

P45983

Informazioni sul gene

human ... MAPK8(5599)

Descrizione generale

Recombinant full-length human JNK1α1/SAPK1c with an N-terminal His-tag

Confezionamento

10 μg vial
Also available in 250μg size (catalog number 14-327M).
Also available in 10 μg size and in bulk

Qualità

Routinely evaluated by phosphorylation of ATF2 (amino acids 19-96)

Descrizione del bersaglio

JNK1α1/SAPK1c

Altre note

For Specific Activity data, refer to the Certificate of Analysis for individual lots of this enzyme.

Note legali

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

Esclusione di responsabilità

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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Pittogrammi

Exclamation mark
GHS07

Avvertenze

Warning

Indicazioni di pericolo

H317

Classi di pericolo

Skin Sens. 1

Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 1

Punto d’infiammabilità (°C)

Not applicable

Certificati d'analisi (COA)

Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘Batch’.

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Girish V Putcha et al.
Neuron, 38(6), 899-914 (2003-06-24)
Trophic factor deprivation (TFD) activates c-Jun N-terminal kinases (JNKs), culminating in coordinate AP1-dependent transactivation of the BH3-only BCL-2 proteins BIM(EL) and HRK, which in turn are critical for BAX-dependent cytochrome c release, caspase activation, and apoptosis. Here, we report that
Y Zhang et al.
The Journal of biological chemistry, 276(24), 20913-20923 (2001-03-30)
Ultraviolet light A (UVA) plays an important role in the etiology of human skin cancer, and UVA-induced signal transduction has a critical role in UVA-induced skin carcinogenesis. The upstream signaling pathways leading to p70(S6K) phosphorylation and activation are not well
S Gupta et al.
The EMBO journal, 15(11), 2760-2770 (1996-06-03)
The JNK protein kinase is a member of the MAP kinase group that is activated in response to dual phosphorylation on threonine and tyrosine. Ten JNK isoforms were identified in human brain by molecular cloning. These protein kinases correspond to
Y Fleming et al.
The Biochemical journal, 352 Pt 1, 145-154 (2000-11-04)
Stress-activated protein kinase 1 (SAPK1), also called c-Jun N-terminal kinase (JNK), becomes activated in vivo in response to pro-inflammatory cytokines or cellular stresses. Its full activation requires the phosphorylation of a threonine and a tyrosine residue in a Thr-Pro-Tyr motif
S Gupta et al.
Science (New York, N.Y.), 267(5196), 389-393 (1995-01-20)
Treatment of cells with pro-inflammatory cytokines or ultraviolet radiation causes activation of the c-Jun NH2-terminal protein kinase (JNK). Activating transcription factor-2 (ATF2) was found to be a target of the JNK signal transduction pathway. ATF2 was phosphorylated by JNK on

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