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Mouse Anti-DAPK2 Recombinant Antibody (3D4) (V2LY-0125-LY1100)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
3D4
Antibody Isotype
IgG1, κ
Application
WB, ELISA

Basic Information

Immunogen
DAPK2 (281-370aa) partial recombinant protein.
Host Species
Mouse
Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal Antibody

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

Format
Liquid
Buffer
PBS
Preservative
None
Concentration
Batch dependent
Purity
>95% as determined by analysis by SDS-PAGE
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
death-associated protein kinase 2
Entrez Gene ID
23604
UniProt ID
Q9UIK4
Function
Calcium/calmodulin-dependent serine/threonine kinase involved in multiple cellular signaling pathways that trigger cell survival, apoptosis, and autophagy. Regulates both type I apoptotic and type II autophagic cell death signals, depending on the cellular setting. The former is caspase-dependent, while the latter is caspase-independent and is characterized by the accumulation of autophagic vesicles. Acts as a mediator of anoikis and a suppressor of beta-catenin-dependent anchorage-independent growth of malignant epithelial cells. May play a role in granulocytic maturation (PubMed:17347302).

Regulates granulocytic motility by controlling cell spreading and polarization (PubMed:24163421).
Biological Process
Anoikis Source: UniProtKB
Apoptotic process Source: UniProtKB
Intracellular signal transduction Source: UniProtKB
Positive regulation of apoptotic process Source: GO_Central
Positive regulation of eosinophil chemotaxis Source: UniProtKB
Positive regulation of neutrophil chemotaxis Source: UniProtKB
Protein autophosphorylation Source: UniProtKB
Protein phosphorylation Source: UniProtKB
Regulation of apoptotic process Source: UniProtKB
Regulation of autophagy Source: UniProtKB
Regulation of intrinsic apoptotic signaling pathway Source: UniProtKB
Cellular Location
Cytoplasm; Autophagosome lumen
More Infomation

Jiang, Y., Liu, J., Xu, H., Zhou, X., He, L., & Zhu, C. (2021). DAPK2 activates NF-κB through autophagy-dependent degradation of I-κBα during thyroid cancer development and progression. Annals of Translational Medicine, 9(13).

Ni, X., Wang, Y., Wang, P., Chu, C., Xu, H., Hu, J., ... & Qi, H. (2020). Death associated protein kinase 2 suppresses TB interactions and GC formation. Molecular immunology, 128, 249-257.

Shiloh, R., Bialik, S., & Kimchi, A. (2019). Ser289 phosphorylation activates both DAPK1 and DAPK2 but in response to different intracellular signaling pathways. Cell cycle, 18(11), 1169-1176.

Wang, Y., Liu, L. L., Tian, Y., Chen, Y., Zha, W. H., Li, Y., & Wu, F. J. (2019). Upregulation of DAPK2 ameliorates oxidative damage and apoptosis of placental cells in hypertensive disorder complicating pregnancy by suppressing human placental microvascular endothelial cell autophagy through the mTOR signaling pathway. International journal of biological macromolecules, 121, 488-497.

Zhou, Q., Wang, L., Chen, H., Xu, B., Xu, W., Sheng, Y., & Duan, Y. (2019). 2, 3′, 4, 4′, 5-pentachlorobiphenyl induced autophagy of the thyrocytes via DAPK2/PKD/VPS34 pathway. Archives of Toxicology, 93(6), 1639-1648.

Elbadawy, M., Usui, T., Yamawaki, H., & Sasaki, K. (2018). Novel functions of death-associated protein kinases through mitogen-activated protein kinase-related signals. International journal of molecular sciences, 19(10), 3031.

Humbert, M., Federzoni, E. A., & Tschan, M. P. (2017). Distinct TP73–DAPK2–ATG5 pathway involvement in ATO‐mediated cell death versus ATRA‐mediated autophagy responses in APL. Journal of leukocyte biology, 102(6), 1357-1370.

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

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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