Product Name: p38g MAPK (180-186) pT183+pY185
Product Number: PE-04BAS00
Size: 200 µg      Price:13.00
      $US
Peptide Name: p38g MAPK (180-186) pT183+pY185

Product Use: This phosphopeptide may be useful as a substrate for screening the phosphatase activity of protein phosphatases and for epitope mapping of phosphosite-specific antibodies. The peptide sequence is located in the protein kinase catalytic domain activation T-loop between subdomains VII and VIII. T183 and Y185 phosphorylation stimulate phosphotransferase activity.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: SEM-pT-G-pY-V

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: Amide

Peptide Modifications Other: Phosphorylated

Peptide Molecular Mass Calculated: 944.82 Da

Peptide Purity Percent after Synthesis and Purification: >50

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Scientific Background: p38g (MAPK12, ERK6) is a protein-serine/threonine kinase of the CMGC group and p38 MAPK family. This kinase is moderate to highly expressed in most tested human tissues except in the pituitary, spinal cord and vagina, where it is notably absent. p38g is activated by phosphorylation at Y185 and probably T183. p38g is activated in response to stress. It has been linked with the development of inflammation, autoimmunity, diabetes and cancer. It functions as a signal transducer during myoblasts to myotubes differentiation. Enforced localization of p38g in the nucleus or cytoplasm markedly attenuates the ability of the kinase to induce cell cycle arrest in fibroblasts. p38g increases basal glucose uptake and decreases DNP- and contraction-stimulated glucose uptake, partially by affecting levels of glucose transporter expression in skeletal muscle. p38g overexpression is linked with highly metastatic breast cancer cell lines, and its expression is associated with the metastatic states of breast tumour samples. The gene was found to be deregulated in uterine leiomyoma. Loss of function may be important to confer survival and inhibit apoptosis for tumour cells.