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Mouse Anti-KCTD13 Recombinant Antibody (3B5) (CBMAB-K0618-LY)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
3B5
Antibody Isotype
IgG2b
Application
WB

Basic Information

Immunogen
Full length human recombinant protein of human KCTD13 produced in E.coli
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!]

Format
Liquid
Concentration
1 mg/mL
Purity
> 95% Purity determined 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
Potassium Channel Tetramerization Domain Containing 13
Introduction
Substrate-specific adapter of a BCR (BTB-CUL3-RBX1) E3 ubiquitin-protein ligase complex required for synaptic transmission (PubMed:19782033). The BCR(KCTD13) E3 ubiquitin ligase complex mediates the ubiquitination of RHOA, leading to its degradation by the proteasome (PubMed:19782033) Degradation of RHOA regulates the actin cytoskeleton and promotes synaptic transmission (By similarity).
Entrez Gene ID
253980
UniProt ID
Q8WZ19
Alternative Names
Potassium Channel Tetramerization Domain Containing 13; Polymerase Delta-Interacting Protein 1; Potassium Channel Tetramerisation Domain Containing 13; BTB/POZ Domain-Containing Protein KCTD13; TNFAIP1-Like Protein; HBACURD1; BACURD1;
Function
Substrate-specific adapter of a BCR (BTB-CUL3-RBX1) E3 ubiquitin-protein ligase complex required for synaptic transmission (PubMed:19782033).
The BCR(KCTD13) E3 ubiquitin ligase complex mediates the ubiquitination of RHOA, leading to its degradation by the proteasome (PubMed:19782033) Degradation of RHOA regulates the actin cytoskeleton and promotes synaptic transmission (By similarity).
Biological Process
Cell migrationManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of Rho protein signal transductionManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of DNA replicationIEA:Ensembl
Positive regulation of synaptic transmissionISS:UniProtKB
Proteasome-mediated ubiquitin-dependent protein catabolic processManual Assertion Based On ExperimentIDA:UniProtKB
Protein homooligomerizationIEA:InterPro
Protein ubiquitinationManual Assertion Based On ExperimentIDA:UniProtKB
Stress fiber assemblyManual Assertion Based On ExperimentIMP:UniProtKB
Cellular Location
Nucleus
Involvement in disease
The gene represented in this entry may act as a disease modifier for autism and schizophrenia associated with recurrent deletions and duplications of chromosome 16p11.2 region (PubMed:22596160, PubMed:25695269).
More Infomation

Gu, J., Ke, P., Guo, H., Liu, J., Liu, Y., Tian, X., ... & Xiao, F. (2023). KCTD13-mediated ubiquitination and degradation of GluN1 regulates excitatory synaptic transmission and seizure susceptibility. Cell Death & Differentiation, 1-16.

Lorenzo, S. M., Moreno, M. D. M. M., Atas, H., Pellen, M., Nalesso, V., Raffelsberger, W., ... & Herault, Y. (2023). Changes in social behavior with MAPK2 and KCTD13/CUL3 pathways alterations in two new outbred rat models for the 16p11. 2 syndromes with autism spectrum disorders. Frontiers in Neuroscience, 17.

Seth, A., Rivera, A., Choi, I. S., Medina-Martinez, O., Lewis, S., O’Neill, M., ... & Lamb, D. J. (2022). Gene dosage changes in KCTD13 result in penile and testicular anomalies via diminished androgen receptor function. FASEB journal: official publication of the Federation of American Societies for Experimental Biology, 36(11), e22567.

Martin Lorenzo, S., Nalesso, V., Chevalier, C., Birling, M. C., & Herault, Y. (2021). Targeting the RHOA pathway improves learning and memory in adult Kctd13 and 16p11. 2 deletion mouse models. Molecular autism, 12, 1-13.

Madison, J. M., Duong, K., Vieux, E. F., Udeshi, N. D., Iqbal, S., Requadt, E., ... & Cottrell, J. R. (2021). Regulation of purine metabolism connects KCTD13 to a metabolic disorder with autistic features. Iscience, 24(1).

Kizner, V., Naujock, M., Fischer, S., Jäger, S., Reich, S., Schlotthauer, I., ... & Gillardon, F. (2020). CRISPR/Cas9-mediated knockout of the neuropsychiatric risk gene KCTD13 causes developmental deficits in human cortical neurons derived from induced pluripotent stem cells. Molecular Neurobiology, 57, 616-634.

Arbogast, T., Razaz, P., Ellegood, J., McKinstry, S. U., Erdin, S., Currall, B., ... & Katsanis, N. (2019). Kctd13-deficient mice display short-term memory impairment and sex-dependent genetic interactions. Human molecular genetics, 28(9), 1474-1486.

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

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