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Mouse Anti-ARID5A Recombinant Antibody (CBYC-A769) (CBMAB-A3560-YC)

Provided herein is a Mouse monoclonal antibody against Human AT-Rich Interaction Domain 5A. The antibody can be used for immunoassay techniques, such as WB.
See all ARID5A antibodies

Summary

Host Animal
Mouse
Specificity
Human, Mouse
Clone
CBYC-A769
Antibody Isotype
IgG2a
Application
WB, FC, IHC

Basic Information

Immunogen
Recombinant protein encompassing a sequence within the center region of human ARID5A.
Specificity
Human, Mouse
Antibody Isotype
IgG2a
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:500-1:10,000
IHC1:100-1:1,000
FC1:50-1:200

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

Format
Liquid
Buffer
PBS
Preservative
None
Concentration
Batch dependent
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
AT-Rich Interaction Domain 5A
Introduction
Members of the ARID protein family, including ARID5A, have diverse functions but all appear to play important roles in development, tissue-specific gene expression, and regulation of cell growth.
Entrez Gene ID
10865
UniProt ID
Q03989
Alternative Names
AT-Rich Interaction Domain 5A; Modulator Recognition Factor 1; AT Rich Interactive Domain 5A (MRF1-Like); ARID Domain-Containing Protein 5A; MRF-1; MRF1;
Function
Binds to AT-rich stretches in the modulator region upstream of the human cytomegalovirus major intermediate early gene enhancer. May act as repressor and down-regulate enhancer-dependent gene expressison (PubMed:8649988).
May positively regulate chondrocyte-specific transcription such as of COL2A1 in collaboration with SOX9 and positively regulate histone H3 acetylation at chondrocyte-specific genes. May stimulate early-stage chondrocyte differentiation and inhibit later stage differention (By similarity).
Can repress ESR1-mediated transcriptional activation; proposed to act as corepressor for selective nuclear hormone receptors (PubMed:15941852).
As RNA-binding protein involved in the regulation of inflammatory response by stabilizing selective inflammation-related mRNAs, such as IL6, STAT3 and TBX21. Binds to stem loop structures located in the 3'UTRs of IL6, STAT3 and TBX21 mRNAs; at least for STAT3 prevents binding of ZC3H12A to the mRNA stem loop structure thus inhibiting its degradation activity. Contributes to elevated IL6 levels possibly implicated in autoimmunity processes. IL6-dependent stabilization of STAT3 mRNA may promote differentiation of naive CD4+ T-cells into T-helper Th17 cells. In CD4+ T-cells may also inhibit RORC-induced Th17 cell differentiation independently of IL6 signaling. Stabilization of TBX21 mRNA contributes to elevated interferon-gamma secretion in Th1 cells possibly implicated in the establishment of septic shock (By similarity).
Stabilizes TNFRSF4/OX40 mRNA by binding to the conserved stem loop structure in its 3'UTR; thereby competing with the mRNA-destabilizing functions of RC3H1 and endoribonuclease ZC3H12A (By similarity).
Biological Process
Cellular response to estrogen stimulus Source: UniProtKB
Innate immune response Source: UniProtKB-KW
Negative regulation of transcription, DNA-templated Source: GDB
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Regulation of transcription by RNA polymerase II Source: GO_Central
Cellular Location
Nucleus
PTM
Phosphorylated by MAPK14 on serine residues involving a TLR4 signaling pathway upon lipopolysaccharide (LPS) stimulation leading to its ubiquitination and proteasomal degradation.
Ubiquitinated leading to proteasomal degradation; involving WWP1 linked to MAPK14-mediated phosphorylation upon LPS stimulation.

Zhou, Q., Zhou, J., & Fan, J. (2021). Expression and prognostic value of ARID5A and its correlation with tumor-infiltrating immune cells in glioma. Frontiers in Oncology, 11, 1839.

Van den Eynde, B. J. (2021). Arid5a: A Missing Link between EMT and Tumoral Immune Resistance. Cancer Immunology Research, 9(8), 854-854.

Parajuli, G., Tekguc, M., Wing, J. B., Hashimoto, A., Okuzaki, D., Hirata, T., ... & Hashimoto, S. (2021). Arid5a promotes immune evasion by augmenting tryptophan metabolism and chemokine expression. Cancer Immunology Research.

Nyati, K. K., Zaman, M. M. U., Sharma, P., & Kishimoto, T. (2020). Arid5a, an RNA-binding protein in immune regulation: RNA stability, inflammation, and autoimmunity. Trends in immunology, 41(3), 255-268.

Sarode, P., Zheng, X., Giotopoulou, G. A., Weigert, A., Kuenne, C., Günther, S., ... & Savai, R. (2020). Reprogramming of tumor-associated macrophages by targeting β-catenin/FOSL2/ARID5A signaling: A potential treatment of lung cancer. Science advances, 6(23), eaaz6105.

Chalise, J. P., Hashimoto, S., Parajuli, G., Kang, S., Singh, S. K., Gemechu, Y., ... & Kishimoto, T. (2019). Feedback regulation of Arid5a and Ppar-γ2 maintains adipose tissue homeostasis. Proceedings of the National Academy of Sciences, 116(30), 15128-15133.

Nyati, K. K., Agarwal, R. G., Sharma, P., & Kishimoto, T. (2019). Arid5a regulation and the roles of Arid5a in the inflammatory response and disease. Frontiers in immunology, 10, 2790.

Higa, M., Oka, M., Fujihara, Y., Masuda, K., Yoneda, Y., & Kishimoto, T. (2018). Regulation of inflammatory responses by dynamic subcellular localization of RNA-binding protein Arid5a. Proceedings of the National Academy of Sciences, 115(6), E1214-E1220.

Hanieh, H., Masuda, K., Metwally, H., Chalise, J. P., Mohamed, M., Nyati, K. K., ... & Kishimoto, T. (2018). Arid5a stabilizes OX40 mRNA in murine CD4+ T cells by recognizing a stem‐loop structure in its 3′ UTR. European journal of immunology, 48(4), 593-604.

Masuda, K., & Kishimoto, T. (2018). A potential therapeutic target RNA-binding protein, Arid5a for the treatment of inflammatory disease associated with aberrant cytokine expression. Current pharmaceutical design, 24(16), 1766-1771.

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

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