|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
Human influenza hemagglutinin (HA) is a surface glycoprotein required for the infectivity of the human virus. The HA tag is derived from the HA-molecule corresponding to amino acids 98-106 has been extensively used as a general epitope tag in expression vectors. Many recombinant proteins have been engineered to express the HA tag, which does not appear to interfere with the bioactivity or the biodistribution of the recombinant protein. This tag facilitates the detection, isolation, and purification of the proteins.
The actual HA tag is as follows: 5' TAC CCA TAC GAT GTT CCA GAT TAC GCT 3' or 5' TAT CCA TAT GAT GTT CCA GAT TAT GCT 3' The amino acid sequence is: YPYDVPDYA.
|Mouse MAPK9 ORF mammalian expression plasmid, C-GFPSpark tag||MG51022-ACG|
|Mouse MAPK9 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG51022-ACR|
|Mouse MAPK9 ORF mammalian expression plasmid, N-GFPSpark tag||MG51022-ANG|
|Mouse MAPK9 ORF mammalian expression plasmid, N-OFPSpark / RFP tag||MG51022-ANR|
|Mouse MAPK9 ORF mammalian expression plasmid, C-Flag tag||MG51022-CF|
|Mouse MAPK9 ORF mammalian expression plasmid, C-His tag||MG51022-CH|
|Mouse MAPK9 ORF mammalian expression plasmid, C-Myc tag||MG51022-CM|
|Mouse MAPK9 ORF mammalian expression plasmid, C-HA tag||MG51022-CY|
|Mouse MAPK9 Gene cDNA clone plasmid||MG51022-G|
|Mouse MAPK9 ORF mammalian expression plasmid, N-Flag tag||MG51022-NF|
|Mouse MAPK9 ORF mammalian expression plasmid, N-His tag||MG51022-NH|
|Mouse MAPK9 ORF mammalian expression plasmid, N-Myc tag||MG51022-NM|
|Mouse MAPK9 ORF mammalian expression plasmid, N-HA tag||MG51022-NY|
|Mouse MAPK9 natural ORF mammalian expression plasmid||MG51022-UT|
|Learn more about expression Vectors|
Mitogen-activated protein kinase 9 (MAPK9), also well known as c-Jun N-terminal kinase (JNK2), is a member of MAP kinase subfamily belonging to the protein kinase superfamily. MAPK9 responds to activation by environmental stress and pro-inflammatory cytokines by phosphorylating a number of 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 suggest 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 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 prevention of vascular disease and atherosclerosis.