Mouse Anti-JMY Recombinant Antibody (CBFYK-007) (CBMAB-0009-FY)

Name: Mouse Anti-JMY Recombinant Antibody (CBFYK-007)
SKU: CBMAB-0009-FY
Rating: 5 (1 reviews)

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Datasheet

SDS

Request for COA

Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Host Animal

Mouse

Clone

CBFYK-007

Application

Specificity

Human

Antibody Isotype

IgG1, 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.

More Infomation

Target

Full Name

junction mediating and regulatory protein, p53 cofactor

Introduction

JMY (Junction Mediating And Regulatory Protein, P53 Cofactor) is a Protein Coding gene. Among its related pathways are Gene Expression and Regulation of TP53 Activity. Gene Ontology (GO) annotations related to this gene include actin binding and transcription coactivator activity. An important paralog of this gene is WHAMM.

Entrez Gene ID

133746

UniProt ID

Q8N9B5

Alternative Names

WHAMM2; WHDC1L3

Function

Acts both as a nuclear p53/TP53-cofactor and a cytoplasmic regulator of actin dynamics depending on conditions (PubMed:30420355).
In nucleus, acts as a cofactor that increases p53/TP53 response via its interaction with p300/EP300. Increases p53/TP53-dependent transcription and apoptosis, suggesting an important role in p53/TP53 stress response such as DNA damage. In cytoplasm, acts as a nucleation-promoting factor for both branched and unbranched actin filaments (PubMed:30420355).
Activates the Arp2/3 complex to induce branched actin filament networks. Also catalyzes actin polymerization in the absence of Arp2/3, creating unbranched filaments (PubMed:30420355).
Contributes to cell motility by controlling actin dynamics. May promote the rapid formation of a branched actin network by first nucleating new mother filaments and then activating Arp2/3 to branch off these filaments. Upon nutrient stress, directly recruited by MAP1LC3B to the phagophore membrane surfaces to promote actin assembly during autophagy (PubMed:30420355).
The p53/TP53-cofactor and actin activator activities are regulated via its subcellular location (By similarity).

Biological Process

de novo' actin filament nucleationISS:UniProtKB
Actin polymerization-dependent cell motilityISS:UniProtKB
Arp2/3 complex-mediated actin nucleationISS:UniProtKB
Cellular response to starvationManual Assertion Based On ExperimentIMP:UniProtKB
DNA repairIEA:UniProtKB-KW
Intrinsic apoptotic signaling pathway by p53 class mediatorISS:UniProtKB
Positive regulation of apoptotic processISS:UniProtKB
Positive regulation of DNA-binding transcription factor activityISS:UniProtKB
Regulation of transcription by RNA polymerase IIISS:HGNC-UCL

Cellular Location

Nucleus; Cytoplasmic vesicle; Cytoplasm, cytoskeleton; Endomembrane system; Cytoplasmic vesicle, autophagosome membrane. Localizes to the nucleus in most cell types. Accumulates in nucleus under DNA damage conditions, increasing p53/TP53 transcription response and reducing its influence on cell motility (By similarity).
In primary neutrophils, it colocalizes with actin filaments at the leading edge and is excluded from the nucleus. Localization correlates with motility, because it moves from the nucleus to the cytoplasmic compartment when cells are differentiated from nonmotile cells into highly motile neutrophil-like cells. Localizes to cytoplasmic vesicles which associate with actin filament and autophagosomal membranes upon starvation-induced autophagy (PubMed:30420355).

PTM

Ubiquitinated by MDM2, leading to its subsequent degradation by the proteasome. In case of DNA damage, the interaction with MDM2 is altered, preventing degradation and allowing interaction with p300/EP300 and its function in p53/TP53 stress response (By similarity).

Rodriguez-Pastrana, I., Birli, E., & Coutts, A. S. (2023). p53-dependent DNA repair during the DNA damage response requires actin nucleation by JMY. Cell Death & Differentiation, 1-12.

Ke, X., Yang, R., Wu, F., Wang, X., Liang, J., Hu, X., & Hu, C. (2021). Exosomal miR-218-5p/miR-363-3p from endothelial progenitor cells ameliorate myocardial infarction by targeting the p53/JMY signaling pathway. Oxidative medicine and cellular longevity, 2021.

Gauthier, L. R., Saati, M., Bensalah-Pigeon, H., Ben M’Barek, K., Gitton-Quent, O., Bertrand, R., ... & Boussin, F. D. (2020). The HIF1α/JMY pathway promotes glioblastoma stem-like cell invasiveness after irradiation. Scientific Reports, 10(1), 18742.

Zuo, W., Guo, W. S., Yu, H. C., Liu, P., & Zhang, Q. D. (2020). Role of Junction‐Mediating and Regulatory Protein in the Pathogenesis of Glucocorticoid‐Induced Endothelial Cell Lesions. Orthopaedic Surgery, 12(3), 964-973.

Lin, Z. L., Li, Y. H., Jin, Y. X., & Kim, N. H. (2019). A Maternal Transcription Factor, Junction Mediating and Regulatory Protein is Required for Preimplantation Development in the Mouse. Development & Reproduction, 23(3), 285.

Liu, X., & Klionsky, D. J. (2019). Regulation of JMY’s actin nucleation activity by TTC5/STRAP and LC3 during autophagy. Autophagy, 15(3), 373-374.

Purnell, M. C. (2019). Bio-Field Array: The Influence of Junction Mediating and Regulatory Protein Expression on Cytoskeletal Filament Behavior During Apoptosis in Triple-Negative Breast Cancer. Breast Cancer: Basic and Clinical Research, 13, 1178223419830981.

Adighibe, O., & Pezzella, F. (2018). The role of JMY in p53 regulation. Cancers, 10(6), 173.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
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Isotype control

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

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