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Mouse Anti-DOCK7 Recombinant Antibody (A-6) (CBMAB-D1486-YC)

Provided herein is a Mouse monoclonal antibody, which binds to Dedicator Of Cytokinesis 7 (DOCK7). The antibody can be used for immunoassay techniques, such as WB, IP, IF, ELISA.
See all DOCK7 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
A-6
Antibody Isotype
IgG
Application
WB, IP, IF, ELISA

Basic Information

Specificity
Human
Antibody Isotype
IgG
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
dedicator of cytokinesis 7
Introduction
DOCK7 is a guanine nucleotide exchange factor (GEF) that plays a role in axon formation and neuronal polarization. The protein displays GEF activity toward RAC1 and RAC3 Rho small GTPases but not toward CDC42.
Entrez Gene ID
85440
UniProt ID
Q96N67
Alternative Names
Dedicator Of Cytokinesis 7; Dedicator Of Cytokinesis Protein 7; KIAA1771; EIEE23; ZIR2;
Function
Functions as a guanine nucleotide exchange factor (GEF), which activates Rac1 and Rac3 Rho small GTPases by exchanging bound GDP for free GTP. Does not have a GEF activity for CDC42. Required for STMN1 'Ser-15' phosphorylation during axon formation and consequently for neuronal polarization (PubMed:16982419).

As part of the DISP complex, may regulate the association of septins with actin and thereby regulate the actin cytoskeleton (PubMed:29467281).

Has a role in pigmentation (By similarity).

Involved in the regulation of cortical neurogenesis through the control of radial glial cells (RGCs) proliferation versus differentiation; negatively regulates the basal-to-apical interkinetic nuclear migration of RGCs by antagonizing the microtubule growth-promoting function of TACC3 (By similarity).
Biological Process
Activation of GTPase activity Source: BHF-UCL
Axonogenesis Source: BHF-UCL
Establishment of neuroblast polarity Source: BHF-UCL
Interkinetic nuclear migration Source: UniProtKB
Microtubule cytoskeleton organization Source: BHF-UCL
Negative regulation of cold-induced thermogenesis Source: YuBioLab
Neuron projection development Source: BHF-UCL
Positive regulation of peptidyl-serine phosphorylation Source: BHF-UCL
Positive regulation of vascular associated smooth muscle cell migration Source: BHF-UCL
Regulation of neurogenesis Source: UniProtKB
Small GTPase mediated signal transduction Source: InterPro
Cellular Location
Axon. Enriched in the developing axons of hippocampal neurons.
Involvement in disease
Developmental and epileptic encephalopathy 23 (DEE23):
A severe disease characterized by early-onset intractable epilepsy, dysmorphic features, intellectual disability, and cortical blindness. Brain imaging shows an abnormally marked pontobulbar sulcus with mild pontine hypoplasia, white matter abnormalities, and atrophy in the occipital lobe.

Kapoor, D., Anand, A., Siddiqui, S., & Sharma, S. (2022). A novel pathogenic variant in DOCK 7 gene in an infant with dysmorphism, epileptic encephalopathy and cortical blindness. Clinical Dysmorphology, 31(1), 39-41.

Gao, M., Guo, G., Huang, J., Hou, X., Ham, H., Kim, W., ... & Lou, Z. (2021). DOCK7 protects against replication stress by promoting RPA stability on chromatin. Nucleic acids research, 49(6), 3322-3337.

Haberlandt, E., Valovka, T., Janjic, T., Müller, T., Blatsios, G., Karall, D., & Janecke, A. R. (2021). Characteristic facial features and cortical blindness distinguish the DOCK7‐related epileptic encephalopathy. Molecular Genetics & Genomic Medicine, 9(3), e1607.

Turkdogan, D., Turkyilmaz, A., Gormez, Z., Sager, G., & Ekinci, G. (2019). A novel truncating mutation of DOCK7 gene with an early-onset non-encephalopathic epilepsy. Seizure-European Journal of Epilepsy, 66, 12-14.

Kukimoto-Niino, M., Tsuda, K., Ihara, K., Mishima-Tsumagari, C., Honda, K., Ohsawa, N., & Shirouzu, M. (2019). Structural basis for the dual substrate specificity of DOCK7 guanine nucleotide exchange factor. Structure, 27(5), 741-748.

Bai, B., Guo, Y. R., Zhang, Y. H., Jin, C. C., Zhang, J. M., Chen, H., & Zhu, B. S. (2019). Novel DOCK7 mutations in a Chinese patient with early infantile epileptic encephalopathy 23. Chinese medical journal, 132(05), 600-603.

Mayer, L., Jasztal, M., Pardo, M., Aguera de Haro, S., Collins, J., Bariana, T. K., ... & Guerrero, J. A. (2018). Nbeal2 interacts with dock7, sec16a, and vac14. Blood, The Journal of the American Society of Hematology, 131(9), 1000-1011.

Li, W. J., Yin, R. X., Cao, X. L., Chen, W. X., Huang, F., & Wu, J. Z. (2018). DOCK7-ANGPTL3 SNPs and their haplotypes with serum lipid levels and the risk of coronary artery disease and ischemic stroke. Lipids in Health and Disease, 17(1), 1-12.

Nakamuta, S., Yang, Y. T., Wang, C. L., Gallo, N. B., Yu, J. R., Tai, Y., & Van Aelst, L. (2017). Dual role for DOCK7 in tangential migration of interneuron precursors in the postnatal forebrain. Journal of Cell Biology, 216(12), 4313-4330.

Le, P. T., Bishop, K. A., Maridas, D. E., Motyl, K. J., Brooks, D. J., Nagano, K., ... & Rosen, C. J. (2017). Spontaneous mutation of Dock7 results in lower trabecular bone mass and impaired periosteal expansion in aged female Misty mice. Bone, 105, 103-114.

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

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