MAP2K1 Antibodies

Dual specificity mitogen-activated protein kinase kinase 1 (MAP2K1)

Dual specificity protein kinase which functions as an important component of the MAP kinase signal transduction pathway. Binding of extracellular ligands such as growth factors, cytokines and hormones for their cell-surface receptors activates RAS and this starts RAF1 activation.

RAF1 then additionally activates the dual-specificity protein kinases MAP2K1/MEK1 and MAP2K2/MEK2. Both MAP2K1/MEK1 and MAP2K2/MEK2 function specifically in the MAPK/ERK cascade, and catalyze the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in the extracellular signal-regulated kinases MAPK3/ERK1 and MAPK1/ERK2, resulting in their activation and additional transduction of the signal inside the MAPK/ERK cascade.

Gene Information

Human
Gene Name:	MAP2K1
Uniprot:	Q02750
Entrez:	5604

Family

Belongs to:
protein kinase superfamily

Alternative Names

dual specificity mitogen-activated protein kinase kinase 1; ERK activator kinase 1; MAP kinase kinase 1; MAP2K1; MAPK/ERK kinase 1; MAPKK1; MEK1; MEK1MAPKK 1; mitogen-activated protein kinase kinase 1; MKK1; MKK1MEK 1; PRKMK1EC 2.7.12.2; protein kinase, mitogen-activated, kinase 1 (MAP kinase kinase 1)

Molecular Weight

Mass (kDA):
43.439 kDA

Genomic Context

Human
Location:	15q22.31
Sequence:	15; NC_000015.10 (66386912..66491544)

Tissue Specificity

Widely expressed, with extremely low levels in brain.

Subcellular Localizations

Cytoplasm, cytoskeleton, microtubule organizing center, centrosome. Cytoplasm, cytoskeleton, microtubule organizing center, spindle pole body. Cytoplasm. Nucleus. Membrane; Peripheral membrane protein. Localizes at centrosomes during prometaphase, midzone during anaphase and midbody during telophase/cytokinesis (PubMed:14737111). Membrane localization is probably regulated by its interaction with KSR1 (PubMed:10409742).

Diseases

• Malignant Neoplasms
• Neoplasms
• Cell Transformation, Neoplastic
• Carcinoma
• Inflammation
• Leukemia
• Tissue Adhesions
• Mammary Neoplasms
• Malignant Neoplasm Of Breast
• Cell Invasion
• Melanoma
• Hyperplasia
• Neoplasm Metastasis

• Malignant Paraganglionic Neoplasm
• Neoplasm Invasiveness
• Tumor Angiogenesis
• Cardio-facio-cutaneous Syndrome
• Malignant Neoplasm Of Lung
• Congenital Heart Defects
• Lung Neoplasms

Interacting Proteins

• BANP
• BIRC6
• BRAF
• BTRC
• MAPK1

• MAPK3
• PIN1
• RAF1
• VRK2
• YAP1

Pathways

• Cell Proliferation
• Cell Cycle
• Cell Death
• Cell Growth
• Secretion
• Localization
• Pathogenesis
• Mapk Cascade
• Angiogenesis
• Cell Migration
• Cell Cycle Arrest
• Cell Differentiation
• Induction Of Apoptosis

• Cytokine Production
• Mitosis
• Cell Activation
• S Phase
• Rna Interference
• Transport
• Senescence

PTMs

• Phosphorylation
• Cleavage
• Dephosphorylation
• Ubiquitination
• Acetylation
• Oxidation
• Biotinylation
• Reduction

• Farnesylation
• Geranylgeranylation
• Myristoylation
• Prenylation
• Ribosylation
• Deacetylation
• Gamma-carboxylation
• Methylation

Research Areas

• Angiogenesis
• Autophagy
• Cancer
• MAP Kinase Signaling
• Phospho-Specific

• Protein Phosphatase
• Signal Transduction
• Tyrosine Kinases

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/MAP2K1

Best Uses Of The MAP2K1 Marker

MAP2K1 is a transporter protein which can identify RR-DTC tumors with low radioiodine levels. Its best uses include identifying metastases lacking radioiodine uptake. Scientists can submit their results for specific species, applications, or samples. They could also be eligible for product credits. This information is accessible to scientists around the world.

MAP2K1 can be used to transport objects

MAP2K1 is a protein that transports fatty acids as well as other oils. Rosai-Dorfman's Disease is more likely to occur when MAP2K1 mutations cause constitutive activation (ERK) downstream. Mutations in this gene can also benefit from targeted therapies. Further research is needed in order to discover the impact of MAP2K1 mutations on Rosai's Dorfman's disease development.

MAP2K1 is one of the members of the MEK family of proteins, which is found in many tissues and cell types. The proteins are part of the RAS/MAPK pathway, which is responsible for transferring chemical signals from the cell's outside to the nucleus. These signals control cell division mobility, self-destruction and cell growth. Because these proteins are so essential for cell growth they are essential for survival.

MAP2K1 interacts with DUSP6 and is a dual-specificity phosphatase. DUSP3 and DUSP6 share the same structure and have a PTP loop and catalytic cysteine. Aspartate D93 and D262 are vital to dephosphorylation reactions, and the catalytic cysteine doesn't get visible on the surface of DUSP6. The MAP2K1 gene transports phospholipids and various metabolic compounds.

Mutations in MAP2K1 are extremely prevalent in cancer patients. It is unclear whether MAP2K1 is the cause of a particular tumor. However genetically modified mice that have aberrant MAP2K1 mutations can be used to further research into cancer etiology. Further research is needed to determine if the mutations are linked to other conditions or are simply as a result of the aging process.

A p-ERK antibody was used to detect MAP2K1 in a subset CLL patients. Three of these patients have mutations in MAP2K1, and four patients did not have any p-ERK expression. A subset of patients with BRAF–WTHCL had no mutations in MAP2K1. They were identified by the presence of ERK-mediated Kinases in their tumor cells.

The MAP2K1 gene regulates a myriad of cell processes, including protein synthesis as well as cell proliferative. The VEGFa/VEGFR2/ERK pathway can be inhibited by MAP2K1 inhibition. This leads to breast cancer cells becoming angiogenic. Additionally, MAP2K1 could be an option for therapeutic targets for cancer. It isn't yet clear what function MAP2K1 has in regulating gene expression or cell survival.

Transporter-based isotopes are able determine RR-DTC metastatic lesions that lack radioiodine uptake

This study provides evidence that the use of transporter-based isotopes can successfully differentiate RR-DTC metastases lacking the ability to uptake radioiodine. The results of this study are described in the accompanying article. For more information, contact the author in question. All authors declare no competing financial interests.

A bilateral laparoscopic bilateral adnexectomy performed under general anesthesia. A 5cm mass was identified intraoperatively in the left side adnexa. The mass was found to be an Ovarian cyst, as determined by an examination of pathology. The condition that was stimulated saw the Tg level drop to 143ng/ml.

Utilizing NIS which is derived from the thyroid hormone, is a reliable and reliable method for identifying RR-DTC metastases without radioiodine uptake. NIS is expressed in epithelial cells of normal tissues, and is the only protein that has been identified to exhibit NIS activity. False-positive lesions may be caused by biological retention, contamination by secretions from the body or a benign thyroid-related lesion. Additionally, false-positive lesions could be caused by dilatation of the biliary duct and thyroid hormone metabolism.

Although MRI imaging is not able to identify RR-DTC metastases that are not radioiodine-uptake deficiencies However, it can be used to evaluate the extent of involvement in the brain. Due to the metabolic process of brain glucose this means that the negative predictive value for brain metastases with 18F-FDG–PET is extremely low. Bone metastases, meanwhile, are predominantly osteolytic and highly vascularized. Occasionally, these metastases are detected on X-ray bone scintigraphy and 18F NaF-PET/CT.

The uptake of 131I also controlled by the salivary glands. The radiopharmacokinetics of 131I in salivary glands change minutely with stimulation and clear rapidly after stimulation. This rapid reaccumulation can be prevented by continuous stimulation. If this process is interrupted, the treatment for RR-DTC metastases can be delayed further.

Efficacy of this therapy is unknown; however, preliminary data on a small clinical series of 13 patients show that it is an effective treatment option for radioiodine-refractory DTC. It eliminates the need for costly multikinase inhibitors and minimizes exposure to patients.