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Mouse Anti-MAPK3 Monoclonal Antibody (3C9) (CBMAB-1195-YC)

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Summary

Host Animal
Mouse
Specificity
Human
Clone
3C9
Antibody Isotype
IgG2a, κ
Application
ELISA, ICC, IF, IHC-P, IP, WB

Basic Information

Immunogen
Partial recombinant protein MAPK3 (AAH13992, aa 279-379) with GST tag
Specificity
Human
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Mitogen-Activated Protein Kinase 3
Introduction
MAPK3 is activated by upstream kinases, resulting in its translocation to the nucleus where it phosphorylates nuclear targets. MAPK3 is a member of the MAP kinase family. MAP kinases, also known as extracellular signal-regulated kinases (ERKs), act in a signaling cascade that regulates various cellular processes such as proliferation, differentiation, and cell cycle progression in response to a variety of extracellular signals.
Entrez Gene ID
UniProt ID
Alternative Names
Mitogen-Activated Protein Kinase 3; Extracellular Signal-Regulated Kinase 1; Microtubule-Associated Protein 2 Kinase; Insulin-Stimulated MAP2 Kinase; MAP Kinase Isoform P44; EC 2.7.11.24; P44-ERK1; P44-MAPK; PRKM3; ERK-1; ERK1;
Function
Serine/threonine kinase which acts as an essential component of the MAP kinase signal transduction pathway. MAPK1/ERK2 and MAPK3/ERK1 are the 2 MAPKs which play an important role in the MAPK/ERK cascade. They participate also in a signaling cascade initiated by activated KIT and KITLG/SCF. Depending on the cellular context, the MAPK/ERK cascade mediates diverse biological functions such as cell growth, adhesion, survival and differentiation through the regulation of transcription, translation, cytoskeletal rearrangements. The MAPK/ERK cascade plays also a role in initiation and regulation of meiosis, mitosis, and postmitotic functions in differentiated cells by phosphorylating a number of transcription factors. About 160 substrates have already been discovered for ERKs. Many of these substrates are localized in the nucleus, and seem to participate in the regulation of transcription upon stimulation. However, other substrates are found in the cytosol as well as in other cellular organelles, and those are responsible for processes such as translation, mitosis and apoptosis. Moreover, the MAPK/ERK cascade is also involved in the regulation of the endosomal dynamics, including lysosome processing and endosome cycling through the perinuclear recycling compartment (PNRC); as well as in the fragmentation of the Golgi apparatus during mitosis. The substrates include transcription factors (such as ATF2, BCL6, ELK1, ERF, FOS, HSF4 or SPZ1), cytoskeletal elements (such as CANX, CTTN, GJA1, MAP2, MAPT, PXN, SORBS3 or STMN1), regulators of apoptosis (such as BAD, BTG2, CASP9, DAPK1, IER3, MCL1 or PPARG), regulators of translation (such as EIAC F4EBP1) and a variety of other signaling-related molecules (like ARHGEF2, FRS2 or GRB10). Protein kinases (such as RAF1, RPS6KA1/RSK1, RPS6KA3/RSK2, RPS6KA2/RSK3, RPS6KA6/RSK4, SYK, MKNK1/MNK1, MKNK2/MNK2, RPS6KA5/MSK1, RPS6KA4/MSK2, MAPKAPK3 or MAPKAPK5) and phosphatases (such as DUSP1, DUSP4, DUSP6 or DUSP16) are other substrates which enable the propagation the MAPK/ERK signal to additional cytosolic and nuclear targets, thereby extending the specificity of the cascade.
Biological Process
Apoptotic processIEA:UniProtKB-KW
Bergmann glial cell differentiationIEA:Ensembl
BMP signaling pathwayManual Assertion Based On ExperimentIMP:BHF-UCL
Cardiac neural crest cell development involved in heart developmentIEA:Ensembl
Cartilage developmentIEA:Ensembl
Caveolin-mediated endocytosisManual Assertion Based On ExperimentTAS:UniProtKB
Cell cycleIEA:UniProtKB-KW
Cell surface receptor signaling pathwayManual Assertion Based On ExperimentIBA:GO_Central
Cellular response to amino acid starvationManual Assertion Based On ExperimentIDA:CAFA
Cellular response to cadmium ionManual Assertion Based On ExperimentIMP:CAFA
Cellular response to dopamineManual Assertion Based On ExperimentIMP:CAFA
Cellular response to mechanical stimulusManual Assertion Based On ExperimentIEP:UniProtKB
Cellular response to reactive oxygen speciesManual Assertion Based On ExperimentIMP:CAFA
Cellular response to tumor necrosis factorIEA:Ensembl
DNA damage induced protein phosphorylationManual Assertion Based On ExperimentIDA:UniProtKB
ERK1 and ERK2 cascadeIEA:Ensembl
Face developmentIEA:Ensembl
Interleukin-1-mediated signaling pathwayManual Assertion Based On ExperimentIMP:BHF-UCL
Intracellular signal transductionManual Assertion Based On ExperimentIBA:GO_Central
Lipopolysaccharide-mediated signaling pathwayIEA:Ensembl
Lung morphogenesisIEA:Ensembl
MAPK cascade1 PublicationNAS:BHF-UCL
Negative regulation of apolipoprotein bindingIEA:Ensembl
Outer ear morphogenesisIEA:Ensembl
Peptidyl-tyrosine autophosphorylationManual Assertion Based On ExperimentIDA:UniProtKB
PhosphorylationManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of cyclase activityManual Assertion Based On ExperimentIMP:CACAO
Positive regulation of ERK1 and ERK2 cascadeManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of gene expressionManual Assertion Based On ExperimentIMP:CAFA
Positive regulation of histone acetylationManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of histone phosphorylationManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of macrophage chemotaxisManual Assertion Based On ExperimentIGI:ARUK-UCL
Positive regulation of macrophage proliferationManual Assertion Based On ExperimentIGI:ARUK-UCL
Positive regulation of protein phosphorylationManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of telomerase activityManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of telomere cappingManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of telomere maintenance via telomeraseManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of transcription by RNA polymerase IIManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of xenophagyIEA:Ensembl
Protein phosphorylationManual Assertion Based On ExperimentIDA:UniProtKB
Regulation of cellular pHIEA:Ensembl
Regulation of cytoskeleton organizationManual Assertion Based On ExperimentTAS:UniProtKB
Regulation of DNA-binding transcription factor activityIEA:Ensembl
Regulation of early endosome to late endosome transportManual Assertion Based On ExperimentTAS:UniProtKB
Regulation of Golgi inheritanceManual Assertion Based On ExperimentTAS:UniProtKB
Regulation of ossificationIEA:Ensembl
Regulation of stress-activated MAPK cascadeManual Assertion Based On ExperimentTAS:UniProtKB
Response to epidermal growth factorManual Assertion Based On ExperimentIDA:UniProtKB
Response to exogenous dsRNAIEA:Ensembl
Sensory perception of painIEA:Ensembl
Stress-activated MAPK cascadeManual Assertion Based On ExperimentIDA:CAFA
Thymus developmentIEA:Ensembl
Thyroid gland developmentIEA:Ensembl
Trachea formationIEA:Ensembl
Transcription, DNA-templatedIEA:Ensembl
Cellular Location
Cytoplasm
Nucleus
Membrane, caveola
Cell junction, focal adhesion
Autophosphorylation at Thr-207 promotes nuclear localization (PubMed:19060905).
PEA15-binding redirects the biological outcome of MAPK3 kinase-signaling by sequestering MAPK3 into the cytoplasm (By similarity).
PTM
Phosphorylated upon KIT and FLT3 signaling (By similarity).
Dually phosphorylated on Thr-202 and Tyr-204, which activates the enzyme. Ligand-activated ALK induces tyrosine phosphorylation. Dephosphorylated by PTPRJ at Tyr-204.
More Infomation

Maradesha, T., Martiz, R. M., Patil, S. M., Prasad, A., Babakr, A. T., Silina, E., ... & Ramu, R. (2023). Integrated network pharmacology and molecular modeling approach for the discovery of novel potential MAPK3 inhibitors from whole green jackfruit flour targeting obesity-linked diabetes mellitus. Plos one, 18(1), e0280847.

Vaziri-Amjad, S., Moradi-Najmi, M., & Taherkhani, A. (2023). Natural Anthraquinones as Promising MAPK3 Inhibitors for Complementary Cancer Therapy. Journal of Chemistry, 2023.

Luo, Y. Y., Zeng, X., Zhu, L., Li, C., Xie, J., Dong, Q., ... & Li, J. Y. (2023). Growth hormone reduces aneuploidy and improves oocytes quality by JAK2-MAPK3/1 pathway in aged mice. Journal of Translational Medicine, 21(1), 426.

Taherkhani, A., Khodadadi, P., Samie, L., Azadian, Z., & Bayat, Z. (2023). Flavonoids as Strong Inhibitors of MAPK3: A Computational Drug Discovery Approach. International Journal of Analytical Chemistry, 2023.

Xie, Y., Ding, M., Yin, X., Wang, G., Zhang, B., Chen, L., ... & Dong, J. (2022). MAPKK2/4/5/7-MAPK3-JAZs modulate phenolic acid biosynthesis in Salvia miltiorrhiza. Phytochemistry, 199, 113177.

Liu, L., Xiao, C., & Sun, Q. (2022). MiRNA-375 inhibits retinoblastoma progression through targeting ERBB2 and inhibiting MAPK1/MAPK3 signalling pathway. Cutaneous and Ocular Toxicology, 41(1), 1-10.

Procházka, R., Bartková, A., Němcová, L., Murín, M., Gad, A., Marcollová, K., ... & Laurinčík, J. (2021). The role of MAPK3/1 and AKT in the acquisition of high meiotic and developmental competence of porcine oocytes cultured in vitro in FLI medium. International Journal of Molecular Sciences, 22(20), 11148.

Liu, J., Wang, X., Yang, L., Nan, W., Ruan, M., & Bi, Y. (2020). Involvement of active MKK9-MAPK3/MAPK6 in increasing respiration in salt-treated Arabidopsis callus. Protoplasma, 257, 965-977.

Du, Y., Zhang, J., Meng, Y., Huang, M., Yan, W., & Wu, Z. (2020). MicroRNA-143 targets MAPK3 to regulate the proliferation and bone metastasis of human breast cancer cells. Amb Express, 10(1), 1-8.

Yu, T. T., Wang, C. Y., & Tong, R. (2020). ERBB2 gene expression silencing involved in ovarian cancer cell migration and invasion through mediating MAPK1/MAPK3 signaling pathway. European Review for Medical & Pharmacological Sciences, 24(10).

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For research use only. Not intended for any clinical use.

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