pdxk-1 Antibody

Characterization of PDXK-1 Antibodies

PDXK-1 antibodies are polyclonal or monoclonal reagents designed to bind specific epitopes of the PDXK protein. Their specificity, cross-reactivity, and applications vary depending on the immunogen and host species.

**2.1. Western Blotting (WB)

PDXK-1 antibodies are widely used to quantify protein levels in lysates. For example:

• ab251802 detected a ~35 kDa band in human plasma and liver tissue, confirming PDXK expression in metabolic organs .

• ab232779 validated PDXK expression in rat pancreas, cerebrum, and spinal cord, highlighting its role in neural and endocrine tissues .

• 15309-1-AP demonstrated PDXK upregulation in spinal cord transection (SCT) models, correlating with neuronal recovery .

**2.2. Immunohistochemistry (IHC)

Antibodies like ab251802 and ab232779 enable spatial mapping of PDXK in tissues:

• ab251802 identified PDXK in human skeletal muscle and cerebral cortex, showing cytoplasmic localization .

• ab232779 visualized PDXK in rat adrenal glands and liver, supporting its role in PLP biosynthesis .

**2.3. Functional Studies

• PDXK shRNA/PDXK ORF: In spinal cord injury models, PDXK knockdown or overexpression altered neuronal survival and locomotor function. PDXK antibodies confirmed protein expression levels in these experiments .

• Mutant PDXK variants: Antibodies detected conformational changes in ATP-binding pockets of D87H, V128I, H246Q, and A243G mutants, linking structural defects to impaired PLP production .

**3.1. Neurological Disorders

• Motor Dysfunction: Overexpression of PDXK in the motor cortex improved locomotor function in SCT rats. PDXK antibodies quantified protein levels, revealing a direct correlation with neuronal survival .

• Polyneuropathy: Biallelic PDXK mutations (e.g., H246Q) caused axonal degeneration and optic atrophy. PDXK antibodies confirmed reduced enzyme activity and PLP levels in erythrocytes, enabling diagnosis .

**3.2. Cancer Research

• Leukemia: PDXK inhibition (e.g., via compound C03) disrupted PLP-dependent pathways, inducing apoptosis in leukemic cells. PDXK antibodies validated target engagement in cytotoxicity assays .

• Genome Instability: PDXK knockout in flies led to chromosome aberrations (CABs), rescuable by PLP supplementation. Human PDXK variants expressed in flies were analyzed using PDXK antibodies to assess rescue efficacy .

Technical Considerations and Limitations

Future Directions

1. Therapeutic Targeting: Developing PDXK inhibitors (e.g., artemisinins) to modulate PLP levels in cancer or neurodegenerative diseases .

2. Biomarker Development: Using PDXK antibodies to monitor PLP deficiency in metabolic disorders or vitamin B6-responsive neuropathies .

3. Structural Studies: Mapping antibody-epitope interactions to guide drug design targeting PDXK’s ATP-binding pocket .