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Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, C-Myc tag

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Human MAPK8 cDNA Clone Product Information
NCBI RefSeq:NM_001278547.1
RefSeq ORF Size:1284bp
cDNA Description:Full length Clone DNA of Homo sapiens mitogen-activated protein kinase 8, transcript variant JNK1-b2 with C terminal Myc tag.
Gene Synonym:JNK, JNK1, PRKM8, SAPK1, JNK1A2, JNK21B1/2
Species:Human
Vector:pCMV3-C-Myc
Plasmid:
Restriction Site:
Tag Sequence:Myc Tag Sequence: GAGCAGAAACTCATCTCAGAAGAGGATCTG
Sequence Description:
Sequencing primers:T7(TAATACGACTCACTATAGGG) BGH(TAGAAGGCACAGTCGAGG)
Promoter:Enhanced CMV mammalian cell promoter
Application:Stable or Transient mammalian expression
Antibiotic in E.coli:Kanamycin
Antibiotic in mammalian cell:Hygromycin
Shipping_carrier:Each tube contains lyophilized plasmid.
Storage:The lyophilized plasmid can be stored at room temperature for three months.
Myc Tag Info

A myc tag is a polypeptide protein tag derived from the c-myc gene product that can be added to a protein using recombinant DNA technology. It can be used for affinity chromatography, then used to separate recombinant, overexpressed protein from wild type protein expressed by the host organism. It can also be used in the isolation of protein complexes with multiple subunits.

A myc tag can be used in many different assays that require recognition by an antibody. If there is no antibody against the studied protein, adding a myc-tag allows one to follow the protein with an antibody against the Myc epitope. Examples are cellular localization studies by immunofluorescence or detection by Western blotting.

The peptide sequence of the myc-tag is: N-EQKLISEEDL-C (1202 Da). It can be fused to the C-terminus and the N-terminus of a protein. It is advisable not to fuse the tag directly behind the signal peptide of a secretory protein, since it can interfere with translocation into the secretory pathway.

Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, C-Myc tag on other vectors
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Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, C-Flag tagHG10795-CF$195
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Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, C-Myc tagHG10795-CM$195
Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, C-HA tagHG10795-CY$195
人 MAPK8 转录变体JNK1-b2 基因全长ORF克隆HG10795-M$75
Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, Flag tagHG10795-M-F$195
Human MAPK8 transcript variant JNK1-b2 natural ORF mammalian expression plasmidHG10795-M-N$195
Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, N-Flag tagHG10795-NF$195
Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, N-His tagHG10795-NH$195
Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, N-Myc tagHG10795-NM$195
Human MAPK8 transcript variant JNK1-b2 ORF mammalian expression plasmid, N-HA tagHG10795-NY$195
Human MAPK8 transcript variant JNK1-b2 natural ORF mammalian expression plasmidHG10795-UT$195
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Background

Mitogen-activated protein kinase 8 (MAPK8), also known as JNK1, is a member of the MAP kinase family. MAP kinases act as an integration point for multiple biochemical signals, and are involved in a wide variety of cellular processes such as proliferation, differentiation, transcription regulation and development. The protein kinases JNK1 has been found to serve as critical molecular links between obesity, metabolic inflammation, and disorders of glucose homeostasis. It is critically involved in the promotion of diet-induced obesity, metabolic inflammation and beta-cell dysfunction. The selective deficiency of JNK1 in the murine nervous system is sufficient to suppress diet-induced obesity. Genetic analysis indicates that the effects of JNK1 can be separated from effects of JNK1 on obesity. JNK1 is a potential pharmacological target for the development of drugs that might be useful for the treatment of metabolic syndrome, and type 2 diabetes. Furthermore, JNK1 plays a major role in the hypoxic cellular damage. JNK1 protein might be an attractive target for antihypoxic therapy in increasing resistance to many pathological conditions and diseases, leading to the oxygen deficit.

References
  • Betigeri S, et al. (2006) JNK1 as a molecular target to limit cellular mortality under hypoxia. Mol Pharm. 3(4): 424-30.
  • Solinas G, et al. (2010) JNK1 and IKKbeta: molecular links between obesity and metabolic dysfunction. FASEB J. 24(8): 2596-611.
  • Sabio G, et al. (2010) Role of the hypothalamic-pituitary-thyroid axis in metabolic regulation by JNK1. Genes Dev. 24(3): 256-64.
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    Catalog: HG10795-CM
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