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Mouse Anti-CDK13 Recombinant Antibody (3G1) (CBMAB-A1393-LY)

The product is antibody recognizes CDC2L5. The antibody 3G1 immunoassay techniques such as: WB, ELISA.
See all CDK13 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
3G1
Antibody Isotype
IgG2a, κ
Application
WB, ELISA

Basic Information

Immunogen
CDC2L5 (AAH01274, 1 a.a. ~ 90 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Specificity
Human
Antibody Isotype
IgG2a, 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
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
Cyclin Dependent Kinase 13
Introduction
The protein encoded by this gene is a member of the cyclin-dependent serine/threonine protein kinase family. Members of this family are well known for their essential roles as master switches in cell cycle control. Some of the cell cycle control kinases are able to phosphorylate proteins that are important for cell differentiation and apoptosis, thus provide connections between cell proliferation, differentiation, and apoptosis. Proteins of this family may also be involved in non-cell cycle-related functions, such as neurocytoskeleton dynamics. The exact function of this protein has not yet been determined. It has unusually large N- and C-termini and is ubiquitously expressed in many tissues. Two alternatively spliced variants are described. [provided by RefSeq]
Entrez Gene ID
8621
UniProt ID
Q14004
Alternative Names
CDC2L; CHED; FLJ35215; KIAA1791
Function
Cyclin-dependent kinase which displays CTD kinase activity and is required for RNA splicing. Has CTD kinase activity by hyperphosphorylating the C-terminal heptapeptide repeat domain (CTD) of the largest RNA polymerase II subunit RPB1, thereby acting as a key regulator of transcription elongation. Required for RNA splicing, probably by phosphorylating SRSF1/SF2. Required during hematopoiesis. In case of infection by HIV-1 virus, interacts with HIV-1 Tat protein acetylated at 'Lys-50' and 'Lys-51', thereby increasing HIV-1 mRNA splicing and promoting the production of the doubly spliced HIV-1 protein Nef.
Biological Process
Alternative mRNA splicing, via spliceosome Source: UniProtKB
Hemopoiesis Source: UniProtKB
Multicellular organism development Source: ProtInc
Negative regulation of stem cell differentiation Source: Ensembl
Neutrophil degranulation Source: Reactome
Phosphorylation of RNA polymerase II C-terminal domain Source: UniProtKB
Positive regulation of cell population proliferation Source: ProtInc
Positive regulation of transcription elongation from RNA polymerase II promoter Source: GO_Central
Protein phosphorylation Source: GO_Central
Regulation of mitotic nuclear division Source: ProtInc
Transcription elongation from RNA polymerase II promoter Source: GO_Central
Viral process Source: UniProtKB-KW
Cellular Location
Nucleus speckle
Involvement in disease
Congenital heart defects, dysmorphic facial features, and intellectual developmental disorder (CHDFIDD): An autosomal dominant syndrome characterized by atrial and/or ventricular septal congenital heart defects, facial dysmorphism with hypertelorism, upslanted palpebral fissures, epicanthal folds, ptosis, strabismus, posteriorly rotated ears, thin upper lip, and small mouth. Patients manifest global developmental delay, delayed walking and speech acquisition, and intellectual disability. Some patients have mild microcephaly, a small cerebral cortex, and agenesis of corpus callosum. More variable features include clinodactyly and/or camptodactyly of the fingers, hypotonia, and joint hypermobility.

Ramírez-Moya, J., Miliotis, C., Baker, A. R., Gregory, R. I., Slack, F. J., & Santisteban, P. (2021). An ADAR1-dependent RNA editing event in the cyclin-dependent kinase CDK13 promotes thyroid cancer hallmarks. Molecular cancer, 20(1), 1-20.

Wang, J., Zhang, Y., Lu, L., Lu, Y., Tang, Q., & Pu, J. (2019). Insight into the molecular mechanism of LINC00152/miR‐215/CDK13 axis in hepatocellular carcinoma progression. Journal of cellular biochemistry, 120(11), 18816-18825.

Baniya, S. (2019). Validating CDK13 as a Novel Dependency in Acute Myeloid Leukemia (Doctoral dissertation, Wellesley College).

Hamilton, M. J., & Suri, M. (2019). CDK13-related disorder. Advances in genetics, 103, 163-182.

Hampl, M., Novakova, M., Kavkova, M., Zikmund, T., Kohoutek, J., Kaiser, J., & Buchtová, M. (2019). Cdk13-/-Mice Exhibit Developmental Delay and Craniofacial Malformations during Embryonic Development.

Quereda, V., Bayle, S., Vena, F., Frydman, S. M., Monastyrskyi, A., Roush, W. R., & Duckett, D. R. (2019). Therapeutic targeting of CDK12/CDK13 in triple-negative breast cancer. Cancer Cell, 36(5), 545-558.

van den Akker, W. M. R., Brummelman, I., Martis, L. M., Timmermans, R. N., Pfundt, R., Kleefstra, T., ... & Schuurs‐Hoeijmakers, J. H. M. (2018). De novo variants in CDK13 associated with syndromic ID/DD: molecular and clinical delineation of 15 individuals and a further review. Clinical genetics, 93(5), 1000-1007.

Uehara, T., Takenouchi, T., Kosaki, R., Kurosawa, K., Mizuno, S., & Kosaki, K. (2018). Redefining the phenotypic spectrum of de novo heterozygous CDK13 variants: Three patients without cardiac defects. European journal of medical genetics, 61(5), 243-247.

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

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