CDKL5
CDKL5, historically named STK9, is the disease-associated member of this family: heterozygous loss-of-function variants in the X-linked CDKL5 gene cause CDKL5 deficiency disorder, an early-onset developmental and epileptic encephalopathy with severe intellectual disability and autistic features. The kinase is expressed in the developing and mature brain, localizes to both nucleus and cytoplasm in a splice-isoform-dependent manner, and phosphorylates microtubule- and synapse-associated proteins implicated in neuronal migration, dendritic arborization, and axonal outgrowth. Activation involves autophosphorylation of the activation segment. Recombinant CDKL5 supports mechanistic studies, characterization of variants of uncertain significance, and screening of inhibitors or gene-therapy constructs for CDKL5-related epilepsy.
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CDKL5 Recombinant Proteins (1)
- Species:
- Source:
Recombinant Protein Expression Service
- Codon Optimization
- Gene Synthesis
- Construction of Expression Vector
- Strain Screening
- Protein Expression
- Purification & QC
- Protein Delivery
- Formel: Human
- Molecular Weight: Sf9 insect cells
The EpCAM/TROP1 protein serves as an important homogeneous interacting molecule that promotes direct contact between intestinal epithelial cells (IEC) and intraepithelial lymphocytes (IEL) in the mucosal epithelium. This feature helps establish an immune barrier against mucosal infections. EpCAM/TROP1 Protein, Human (His-SUMO) is the recombinant human-derived EpCAM/TROP1 protein, expressed by E. coli , with N-6*His, N-SUMO labeled tag.
