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Mouse Anti-DTNA Recombinant Antibody (1B11) (CBMAB-D1834-YC)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
1B11
Antibody Isotype
IgG2b
Application
FC

Basic Information

Immunogen
Full length human recombinant protein of human DTNA (NP_116761) produced in HEK293T cell.
Specificity
Human
Antibody Isotype
IgG2b
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!]

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
Dystrobrevin Alpha
Introduction
DTNA belongs to the dystrobrevin subfamily of the dystrophin family. This protein is a component of the dystrophin-associated protein complex (DPC), which consists of dystrophin and several integral and peripheral membrane proteins, including dystroglycans, sarcoglycans, syntrophins and alpha- and beta-dystrobrevin. The DPC localizes to the sarcolemma and its disruption is associated with various forms of muscular dystrophy. Mutations in this gene are associated with left ventricular noncompaction with congenital heart defects.
Entrez Gene ID
1837
UniProt ID
Q9Y4J8
Alternative Names
Dystrobrevin Alpha; Dystrophin-Related Protein 3; DTN-A; DRP3; Dystrobrevin, Alpha; Alpha-Dystrobrevin; D18S892E; LVNC1; DTN;
Research Area
May be involved in the formation and stability of synapses as well as being involved in the clustering of nicotinic acetylcholine receptors.
Biological Process
Chemical synaptic transmission Source: ProtInc
Neuromuscular synaptic transmission Source: ProtInc
Signal transduction Source: ProtInc
Striated muscle contraction Source: ProtInc
Synaptic signaling Source: GO_Central
Cellular Location
Cell membrane; Cytoplasm; Synapse. In peripheral nerves, colocalizes with MAGEE1 in the Schwann cell membrane.
Involvement in disease
Left ventricular non-compaction 1 (LVNC1):
A form of left ventricular non-compaction, a cardiomyopathy due to myocardial morphogenesis arrest and characterized by a hypertrophic left ventricle, a severely thickened 2-layered myocardium, numerous prominent trabeculations, deep intertrabecular recesses, and poor systolic function. Clinical manifestations are variable. Some affected individuals experience no symptoms at all, others develop heart failure. In some cases, left ventricular non-compaction is associated with other congenital heart anomalies. LVNC1 is an autosomal dominant condition.
PTM
Phosphorylation of DTN-1 on tyrosine kinase substrate domain present in the C-terminus.
More Infomation

Malakootian, M., Jalilian, M., Kalayinia, S., Hosseini Moghadam, M., Heidarali, M., & Haghjoo, M. (2022). Whole-exome sequencing reveals a rare missense variant in DTNA in an Iranian pedigree with early-onset atrial fibrillation. BMC cardiovascular disorders, 22(1), 1-9.

Fu, G., Pei, Z., & Song, N. (2021). Oncogenic microRNA-301b regulates tumor repressor dystrobrevin alpha to facilitate cell growth, invasion and migration in esophageal cancer. Esophagus, 18(2), 315-325.

Tsoumpra, M. K., Sawatsubashi, S., Imamura, M., Fukumoto, S., Takeda, S. I., Matsumoto, T., & Aoki, Y. (2020). Dystrobrevin alpha gene is a direct target of the vitamin D receptor in muscle. Journal of Molecular Endocrinology, 64(3), 195-208.

Hu, Z. G., Zhang, S., Chen, Y. B., Cao, W., Zhou, Z. Y., Zhang, J. N., ... & He, S. Q. (2020). DTNA promotes HBV-induced hepatocellular carcinoma progression by activating STAT3 and regulating TGFβ1 and P53 signaling. Life Sciences, 258, 118029.

Zhao, Z., Zhao, Y., Ying‐Chun, L., Zhao, L., Zhang, W., & Yang, J. G. (2019). Protective role of microRNA‐374 against myocardial ischemia‐reperfusion injury in mice following thoracic epidural anesthesia by downregulating dystrobrevin alpha‐mediated Notch1 axis. Journal of Cellular Physiology, 234(7), 10726-10740.

Li, N., Tang, Y., Liu, B., Cong, W., Liu, C., & Xiao, J. (2017). Retinoid acid-induced microRNA-27b-3p impairs C2C12 myoblast proliferation and differentiation by suppressing α-dystrobrevin. Experimental Cell Research, 350(2), 301-311.

Cao, Q., Shen, Y., Liu, X., Yu, X., Yuan, P., Wan, R., ... & Hong, K. (2017). Phenotype and functional analyses in a transgenic mouse model of left ventricular noncompaction caused by a DTNA mutation. International Heart Journal, 16-019.

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

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