Rabbit anti-Human PARD6A Polyclonal Antibody

Uniprot Id

Q9NPB6

Target Species

Human

Target Name

PARD6A

Target Full Name

Partitioning defective 6 homolog alpha

Target Function

Adapter protein involved in asymmetrical cell division and cell polarization processes. Probably involved in the formation of epithelial tight junctions. Association with PARD3 may prevent the interaction of PARD3 with F11R/JAM1, thereby preventing tight junction assembly. The PARD6-PARD3 complex links GTP-bound Rho small GTPases to atypical protein kinase C proteins. Regulates centrosome organization and function. Essential for the centrosomal recruitment of key proteins that control centrosomal microtubule organization.

Target Subcellular Location

Cytoplasm. Cell membrane. Cell projection, ruffle. Cell junction, tight junction. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome, centriolar satellite. Cytoplasm, cytoskeleton, microtubule organizing center, centrosome.

Target Protein Families

PAR6 family

Target Tissue Specificity

Expressed in pancreas, skeletal muscle, brain and heart. Weakly expressed in kidney and placenta.

Target Synonyms

0710008C04Rik; 2610010A15Rik; Par 6 partitioning defective 6 C elegans homolog alpha; Par 6 partitioning defective 6 homolog alpha; Par 6 partitioning defective 6 homolog alpha C elegans; PAR 6A; PAR-6 alpha; PAR-6; par-6 family cell polarity regulator alpha; PAR-6A; PAR6; PAR6A_HUMAN; PAR6alpha; PAR6C; Pard6a; Partitioning defective 6 homolog alpha; partitioning-defective protein 6; partitioning-defective protein 6, C. elegans, homolog of, alpha; Tax interacting protein 40; Tax interaction protein 40; TAX40; TIP 40; TIP-40; TIP40

Target Background

This gene is a member of the PAR6 family and encodes a protein with a PSD95/Discs-large/ZO1 (PDZ) domain and a semi-Cdc42/Rac interactive binding (CRIB) domain. This cell membrane protein is involved in asymmetrical cell division and cell polarization processes as a member of a multi-protein complex. The protein also has a role in the epithelial-to-mesenchymal transition (EMT) that characterizes the invasive phenotype associated with metastatic carcinomas. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.