JNK2 Protein, Human, Recombinant (His)

Catalog No. TMPY-04550

Synonyms: JNK2α, SAPK1a, PRKM9, JNK2β, JNK2, SAPK, JNK2BETA, mitogen-activated protein kinase 9, JNK2ALPHA, JNK-55, p54aSAPK, JNK2B, JNK2A, p54a

Mitogen-activated protein kinase 9 (MAPK9), also well known as c-Jun N-terminal kinase (JNK2), is a member of the MAP kinase subfamily belonging to the protein kinase superfamily. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating some transcription factors, such as c-Jun and ATF2. The crystal structure of human JNK2 complexed with an indazole inhibitor by applying a high-throughput protein engineering and surface-site mutagenesis approach. A novel conformation of the activation loop is observed, which is not compatible with its phosphorylation by upstream kinases. This activation inhibitory conformation of JNK2 is stabilized by the MAP kinase insert that interacts with the activation loop in an induced-fit manner. It suggests that the MAP kinase insert of JNK2 plays a role in the regulation of JNK2 activation, possibly by interacting with intracellular binding partners. JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation, and suggests that JNK2 is a negative regulator of cellular proliferation in multiple cell types. JNK2 prevents replicative stress by coordinating cell cycle progression and DNA damage repair mechanisms. JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. JNK2 negatively regulates antigen-specific CD8+ T cell expansion and effector function, and thus selectively blocking JNK2 in CD8+ T cells may potentially enhance the anti-tumor immune response. Lack of JNK2 expression was associated with higher tumor aneuploidy and reduced DNA damage response. Additionally, the JNK2 protein could be a novel therapeutic target in dry eye disease and may provide a novel target for the prevention of vascular disease and atherosclerosis.

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JNK2 Protein, Human, Recombinant (His)

Pack Size	Availability	Price/USD	Quantity
50 μg	5 days	$ 498.00
500 μg	5 days	$ 3,270.00

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DATASHEET SDS

Biological Description

Technical Params

Product Properties

References and Literature

Description

Species	Human
Expression System	Baculovirus-Insect Cells
Tag	His
Accession Number	P45984-1
Synonyms	JNK2α, SAPK1a, PRKM9, JNK2β, JNK2, SAPK, JNK2BETA, mitogen-activated protein kinase 9, JNK2ALPHA, JNK-55, p54aSAPK, JNK2B, JNK2A, p54a
Construction	A DNA sequence encoding the full length of human MAPK9 (NP_002743.3) (Met 1-Arg 424) was fused with a polyhistidine tag at the C-terminus.
Protein Purity	> 90 % as determined by SDS-PAGE
Molecular Weight	49.5 kDa (predicted)

Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Formulation	Lyophilized from sterile 50mM Tris, 100mM NaCl, pH 8.0, 10% glycerol, 0. 5mM EDTA, 0. 5mM PMSFPlease contact us for any concerns or special requirements. Normally 5 % - 8 % trehalose, mannitol and 0. 01% Tween 80 are added as protectants before lyophilization. Please refer to the specific buffer information in the hard copy of CoA.
Reconstitution	A hardcopy of datasheet with reconstitution instructions is sent along with the products. Please refer to it for detailed information.
Stability & Storage	Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Shipping	In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
Research Background	Mitogen-activated protein kinase 9 (MAPK9), also well known as c-Jun N-terminal kinase (JNK2), is a member of the MAP kinase subfamily belonging to the protein kinase superfamily. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating some transcription factors, such as c-Jun and ATF2. The crystal structure of human JNK2 complexed with an indazole inhibitor by applying a high-throughput protein engineering and surface-site mutagenesis approach. A novel conformation of the activation loop is observed, which is not compatible with its phosphorylation by upstream kinases. This activation inhibitory conformation of JNK2 is stabilized by the MAP kinase insert that interacts with the activation loop in an induced-fit manner. It suggests that the MAP kinase insert of JNK2 plays a role in the regulation of JNK2 activation, possibly by interacting with intracellular binding partners. JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation, and suggests that JNK2 is a negative regulator of cellular proliferation in multiple cell types. JNK2 prevents replicative stress by coordinating cell cycle progression and DNA damage repair mechanisms. JNK2 blocks the ubiquitination of tumor suppressor p53, and thus increases the stability of p53 in nonstressed cells. JNK2 negatively regulates antigen-specific CD8+ T cell expansion and effector function, and thus selectively blocking JNK2 in CD8+ T cells may potentially enhance the anti-tumor immune response. Lack of JNK2 expression was associated with higher tumor aneuploidy and reduced DNA damage response. Additionally, the JNK2 protein could be a novel therapeutic target in dry eye disease and may provide a novel target for the prevention of vascular disease and atherosclerosis.

References and Literature

1. Sabapathy K,et al.(2004) JNK2: a negative regulator of cellular proliferation. Cell Cycle. 3(12): 1520-3. 2. Tao J,et al.(2007) JNK2 negatively regulates CD8+ T cell effector function and anti-tumor immune response. Eur J Immunol. 37(3): 818-29. 3. Shaw D,et al.(2008) The crystal structure of JNK2 reveals conformational flexibility in the MAP kinase insert and indicates its involvement in the regulation of catalytic activity. J Mol Biol. 383(4): 885-93. 4. Osto E,et al.(2008) c-Jun N-terminal kinase 2 deficiency protects against hypercholesterolemia-induced endothelial dysfunction and oxidative stress. 118(20): 2073-80. 5. De Paiva CS,et al.(2009) Essential role for c-Jun N-terminal kinase 2 in corneal epithelial response to desiccating stress. Arch Ophthalmol. 127(12): 1625-31. 6. Chen P,et al.(2010) Jnk2 effects on tumor development, genetic instability and replicative stress in an oncogene-driven mouse mammary tumor model. PLoS One. 5(5): e10443.

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Keywords

JNK2 Protein, Human, Recombinant (His) JNK2α JNK 55 SAPK1a PRKM9 JNK2β PRKM-9 JNK2 SAPK JNK-2 JNK2BETA PRKM 9 mitogen-activated protein kinase 9 JNK55 JNK2ALPHA JNK-55 p54aSAPK JNK 2 JNK2B JNK2A p54a recombinant recombinant-proteins proteins protein