The antiserum was produced against synthesized peptide derived from human MEK-2 around the phosphorylation site of Thr394. AA range:261-310

Phospho-MEK-2 (T394) Polyclonal Antibody detects endogenous levels of MEK-2 protein only when phosphorylated at T394.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):PGtPT

MAP2K2

Dual specificity mitogen-activated protein kinase kinase 2

MAP2K2 ;
MEK2 ;
MKK2 ;
PRKMK2 ;
Dual specificity mitogen-activated protein kinase kinase 2 ;
MAP kinase kinase 2 ;
MAPKK 2 ;
ERK activator kinase 2 ;
MAPK/ERK kinase 2 ;
MEK 2

The protein encoded by this gene is a dual specificity protein kinase that belongs to the MAP kinase kinase family. This kinase is known to play a critical role in mitogen growth factor signal transduction. It phosphorylates and thus activates MAPK1/ERK2 and MAPK2/ERK3. The activation of this kinase itself is dependent on the Ser/Thr phosphorylation by MAP kinase kinase kinases. Mutations in this gene cause cardiofaciocutaneous syndrome (CFC syndrome), a disease characterized by heart defects, mental retardation, and distinctive facial features similar to those found in Noonan syndrome. The inhibition or degradation of this kinase is also found to be involved in the pathogenesis of Yersinia and anthrax. A pseudogene, which is located on chromosome 7, has been identified for this gene. [provided by RefSeq, Jul 2008],

Catalytic activity:ATP + a protein = ADP + a phosphoprotein.,Disease:Defects in MAP2K2 are a cause of cardiofaciocutaneous syndrome (CFC syndrome) [MIM:115150]; also known as cardio-facio-cutaneous syndrome. CFC syndrome is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy. Some affected individuals present with ectodermal abnormalities such as sparse, friable hair, hyperkeratotic skin lesions and a generalized ichthyosis-like condition. Typical facial features are similar to Noonan syndrome. They include high forehead with bitemporal constriction, hypoplastic supraorbital ridges, downslanting palpebral fissures, a depressed nasal bridge, and posteriorly angulated ears with prominent helices. The inheritance of CFC syndrome is autosomal dominant.,Function:Catalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. Activates the ERK1 and ERK2 MAP kinases.,PTM:MAPKK is itself dependent on Ser/Thr phosphorylation for activity catalyzed by MAP kinase kinase kinases (RAF or MEKK1).,similarity:Belongs to the protein kinase superfamily. STE Ser/Thr protein kinase family. MAP kinase kinase subfamily.,similarity:Contains 1 protein kinase domain.,subunit:Interacts with MORG1.,

Cytoplasm . Membrane ; Peripheral membrane protein . Membrane localization is probably regulated by its interaction with KSR1. .

Colon carcinoma,Epithelium,Human cerebellum,Muscle,Platelet

>>EGFR tyrosine kinase inhibitor resistance ;
>>Endocrine resistance ;
>>MAPK signaling pathway ;
>>ErbB signaling pathway ;
>>Ras signaling pathway ;
>>Rap1 signaling pathway ;
>>cGMP-PKG signaling pathway ;
>>cAMP signaling pathway ;
>>HIF-1 signaling pathway ;
>>FoxO signaling pathway ;
>>Sphingolipid signaling pathway ;
>>Phospholipase D signaling pathway ;
>>Autophagy - animal ;
>>mTOR signaling pathway ;
>>PI3K-Akt signaling pathway ;
>>Apoptosis ;
>>Cellular senescence ;
>>Vascular smooth muscle contraction ;
>>VEGF signaling pathway ;
>>Apelin signaling pathway ;
>>Gap junction ;
>>Signaling pathways regulating pluripotency of stem cells ;
>>Neutrophil extracellular trap formation ;
>>Toll-like receptor signaling pathway ;
>>Natural killer cell mediated cytotoxicity ;
>>T cell receptor signaling pathway ;
>>B cell receptor signaling pathway ;
>>Fc epsilon RI signaling pathway ;
>>Long-term potentiation ;
>>Neurotrophin signaling pathway ;
>>Long-term depression ;
>>Regulation of actin cytoskeleton ;
>>Insulin signaling pathway ;
>>GnRH signaling pathway ;
>>Estrogen signaling pathway ;
>>Melanogenesis ;
>>Prolactin signaling pathway ;
>>Thyroid hormone signaling pathway ;
>>Oxytocin signaling pathway ;
>>Relaxin signaling pathway ;
>>GnRH secretion ;
>>Cushing syndrome ;
>>Growth hormone synthesis, secretion and action ;
>>Alzheimer disease ;
>>Pathways of neurodegeneration - multiple diseases ;
>>Salmonella infection ;
>>Yersinia infection ;
>>Hepatitis C ;
>>Hepatitis B ;
>>Human cytomegalovirus infection ;
>>Influenza A ;
>>Human papillomavirus infection ;
>>Human T-cell leukemia virus 1 infection ;
>>Kaposi sarcoma-associated herpesvirus infection ;
>>Human immunodeficiency virus 1 infection ;
>>Pathways in cancer ;
>>Proteoglycans in cancer ;
>>MicroRNAs in cancer ;
>>Chemical carcinogenesis - receptor activation ;
>>Chemical carcinogenesis - reactive oxygen species ;
>>Colorectal cancer ;
>>Renal cell carcinoma ;
>>Endometrial cancer ;
>>Glioma ;
>>Prostate cancer ;
>>Thyroid cancer ;
>>Melanoma ;
>>Bladder cancer ;
>>Chronic myeloid leukemia ;
>>Acute myeloid leukemia ;
>>Non-small cell lung cancer ;
>>Breast cancer ;
>>Hepatocellular carcinoma ;
>>Gastric cancer ;
>>Central carbon metabolism in cancer ;
>>Choline metabolism in cancer ;
>>PD-L1 expression and PD-1 checkpoint pathway in cancer