Product Overview
Description
CLPP-00150395 is recombinant human CDK13 protein
Applications
ELISA, Western Blot
Protein Length
Protein fragment
Nature
Recombinant Protein
Sequence
MLPEDKEADSLRGNISVKAVKKEVEKKLRCLLADLPLPPELPGGDDLSKSPEEKKTATQLHSKRRPKICGPRYGETKEKDIDWGKRCVDK
Sequence Similarities
Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily. Contains 1 protein kinase domain.
Target Information
Alternative Names
CDC2 related protein kinase 5; CDC2-related protein kinase 5; CDC2L; CDK13; CDK13_HUMAN; cell division controller cholinesterase related; cell division cycle 2 like 5; cell division cycle 2 like 5 (cholinesterase related cell division controller); Cell division cycle 2 like protein kinase 5; Cell division cycle 2-like protein kinase 5; Cell division protein kinase 13; CHED; Cholinesterase related cell division controller; Cholinesterase-related cell division controller; cyclin dependent kinase 13; Cyclin-dependent kinase 13; hCDK13
Protein 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.
Tissue Specificity
Expressed in fetal brain, liver, muscle and in adult brain. Also expressed in neuroblastoma and glioblastoma tumors.
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. The disease is caused by variants affecting the gene represented in this entry.
Shipping & Handling
Constituents
0.31% Glutathione, 0.79% Tris HCl.
Shipping
Shipped on dry ice.
