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Mouse Anti-NFATC1 Recombinant Antibody (CBWJN-0765) (CBMAB-N0295-WJ)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
CBWJN-0765
Antibody Isotype
IgG2a, κ
Application
ELISA, WB

Basic Information

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
Concentration
1 mg/mL
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
NFATC1
Introduction
The product of this gene is a component of the nuclear factor of activated T cells DNA-binding transcription complex. This complex consists of at least two components: a preexisting cytosolic component that translocates to the nucleus upon T cell receptor (TCR) stimulation, and an inducible nuclear component. Proteins belonging to this family of transcription factors play a central role in inducible gene transcription during immune response. The product of this gene is an inducible nuclear component. It functions as a major molecular target for the immunosuppressive drugs such as cyclosporin A. Multiple alternatively spliced transcript variants encoding distinct isoforms have been identified for this gene. Different isoforms of this protein may regulate inducible expression of different cytokine genes. [provided by RefSeq, Jul 2013]
Entrez Gene ID
4772
UniProt ID
O95644
Alternative Names
Nuclear Factor Of Activated T Cells 1; Nuclear Factor Of Activated T-Cells, Cytoplasmic, Calcineurin-Dependent 1; NFAT Transcription Complex Cytosolic Component; Nuclear Factor Of Activated T-Cells 1; NF-ATC; NFAT2; NFATc;
Function
Plays a role in the inducible expression of cytokine genes in T-cells, especially in the induction of the IL-2 or IL-4 gene transcription. Also controls gene expression in embryonic cardiac cells. Could regulate not only the activation and proliferation but also the differentiation and programmed death of T-lymphocytes as well as lymphoid and non-lymphoid cells (PubMed:10358178).

Required for osteoclastogenesis and regulates many genes important for osteoclast differentiation and function (By similarity).
Biological Process
Aortic valve morphogenesis Source: BHF-UCL
Calcineurin-NFAT signaling cascade Source: UniProtKB
Intracellular signal transduction Source: MGI
Negative regulation of vascular associated smooth muscle cell differentiation Source: BHF-UCL
Negative regulation of Wnt signaling pathway Source: ParkinsonsUK-UCL
Positive regulation of transcription, DNA-templated Source: UniProtKB
Positive regulation of transcription by RNA polymerase II Source: UniProtKB
Pulmonary valve morphogenesis Source: BHF-UCL
Regulation of transcription by RNA polymerase II Source: GO_Central
Cellular Location
Nucleus
Cytoplasm
Note: Cytoplasmic for the phosphorylated form and nuclear after activation that is controlled by calcineurin-mediated dephosphorylation. Rapid nuclear exit of NFATC is thought to be one mechanism by which cells distinguish between sustained and transient calcium signals. The subcellular localization of NFATC plays a key role in the regulation of gene transcription (PubMed:16511445). Nuclear translocation of NFATC1 is enhanced in the presence of TNFSF11. Nuclear translocation is decreased in the presence of FBN1 which can bind and sequester TNFSF11 (By similarity).
PTM
Phosphorylated by NFATC-kinase and GSK3B; phosphorylation induces NFATC1 nuclear exit and dephosphorylation by calcineurin promotes nuclear import. Phosphorylation by PKA and DYRK2 negatively modulates nuclear accumulation, and promotes subsequent phosphorylation by GSK3B or casein kinase 1.
More Infomation

Zheng, H., Liu, Y., Deng, Y., Li, Y., Liu, S., Yang, Y., ... & Yu, H. (2024). Recent advances of NFATc1 in rheumatoid arthritis-related bone destruction: mechanisms and potential therapeutic targets. Molecular Medicine, 30(1), 1-23.

Omata, Y., Tachibana, H., Aizaki, Y., Mimura, T., & Sato, K. (2023). Essentiality of Nfatc1 short isoform in osteoclast differentiation and its self-regulation. Scientific reports, 13(1), 18797.

Jin, F., Zhu, Y., Liu, M., Wang, R., Cui, Y., Wu, Y., ... & Ren, Z. (2022). Babam2 negatively regulates osteoclastogenesis by interacting with Hey1 to inhibit Nfatc1 transcription. International Journal of Biological Sciences, 18(11), 4482.

Wang, J., Zhao, Q., Fu, L., Zheng, S., Wang, C., Han, L., ... & Zhang, Y. (2022). CD301b+ macrophages mediate angiogenesis of calcium phosphate bioceramics by CaN/NFATc1/VEGF axis. Bioactive Materials, 15, 446-455.

Gunawan, F., Gentile, A., Gauvrit, S., Stainier, D. Y., & Bensimon-Brito, A. (2020). Nfatc1 promotes interstitial cell formation during cardiac valve development in zebrafish. Circulation research, 126(8), 968-984.

Kang, J. Y., Kang, N., Yang, Y. M., Hong, J. H., & Shin, D. M. (2020). The role of Ca2+-NFATc1 signaling and its modulation on osteoclastogenesis. International journal of molecular sciences, 21(10), 3646.

Gu, W., Wang, Z., Sun, Z., Bao, Z., Zhang, L., Geng, Y., ... & Li, L. (2020). Role of NFATc1 in the bone-vascular axis calcification paradox. Journal of Cardiovascular Pharmacology, 75(3), 200-207.

Xiao, Y., Qureischi, M., Dietz, L., Vaeth, M., Vallabhapurapu, S. D., Klein-Hessling, S., ... & Berberich-Siebelt, F. (2020). Lack of NFATc1 SUMOylation prevents autoimmunity and alloreactivity. Journal of Experimental Medicine, 218(1), e20181853.

Yang, Y., Chung, M. R., Zhou, S., Gong, X., Xu, H., Hong, Y., ... & Jiang, L. (2019). STAT3 controls osteoclast differentiation and bone homeostasis by regulating NFATc1 transcription. Journal of Biological Chemistry, 294(42), 15395-15407.

Liu, Y., Wang, C., Wang, G., Sun, Y., Deng, Z., Chen, L., ... & Xu, J. (2019). Loureirin B suppresses RANKL-induced osteoclastogenesis and ovariectomized osteoporosis via attenuating NFATc1 and ROS activities. Theranostics, 9(16), 4648.

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

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