PARD3

Official Full Name

par-3 family cell polarity regulator

Organism

Homo sapiens

GeneID

56288

Background

This gene encodes a member of the PARD protein family. PARD family members interact with other PARD family members and other proteins; they affect asymmetrical cell division and direct polarized cell growth. Multiple alternatively spliced transcript variants have been described for this gene. [provided by RefSeq, Oct 2011]

Synonyms

Baz; ASIP; PAR3; PARD-3; PARD3A; SE2-5T2; PPP1R118; SE2-5L16; SE2-5LT1; PAR3alpha;

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Detailed Information

The association between PARD3 and cancer

As a member of the Par polarity complex, partition defective 3 (PARD3) is also known as ASIP (atypical protein kinase C (aPKC)-specific-interacting protein). In the zygote of the nematode Caenorhabditis elegans (aka PAR3), role of PARD3 in polarity was first characterized. And it was found to affect ACD during embryonic development by establishing anterior-posterior polarity. In various spatial asymmetry required cellular processes of vertebrates, such as migration and ACD, PARD3 plays significant roles in its regulation. More than this, it also forms a dynamic complex with other Par complex proteins, such as aPKC and PARD6, to be functional in the assembly of tight junctions in epithelial tissues. In non-epithelial tissues, such as neurons, in which PARD3 establishes polarity and ACD, and its expression is polarized in activated T cells when in contract with an antigen presenting cell.

Three PARD3 isoforms with molecular weights of 180, 150, and 100 kDa are encoded by the same gene on chromosome 10. Developed from the alternative splicing, these isoforms are differentially expressed in tissues, in murine heart and kidney tissues, all the isoforms are expressed, while only 180 and 100 kDa isoforms are detectable in murine brain. In humans, there is a strong expression in skeletal muscle, kidney and lung while only 100 kDa isoform is highly expressed in placenta and liver. The PARD3 protein has four domains for its composition: a conserved region 1 (CR1) at the N-terminal, three PDZ protein-binding domains (CR2) and one aPKC-binding domain (CR3) at the C-terminal followed by a coiled-coil region. Localization of PARD3 to the apical site of tight junctions in mammalian epithelial tissues is relied on the functionality of the CR1 region and the amino acids 937-1024 in the coiled-coil region, whose mutation can arise a diffuse distribution of PARD3 into the cytosol. Large PARD3 oligomeric complexes formed by PARD3 self-association under the facilitation of the CR1 region is essential for membrane targeting.

The association between PARD3 deregulation and cancer development has been examined in many studies for its involvement in maintaining the 3D architecture of tissues, in addition to this, PARD3 has been concluded as a tumor suppressor or an onco-protein in various types of epithelial cancers in the last two decades. The report of these two functions opposite to each other in other polarity proteins may highlight their tissue-dependent activity.

Figure 1. PARD3 promotes the interaction between PP1A and LATS to induce LATS inactivation, therefore leading to TAZ dephosphorylation and activation (Xiao, et al, 2015)

References:

Lv, Xian‐Bo, et al. PARD 3 induces TAZ activation and cell growth by promoting LATS 1 and PP 1 interaction. EMBO reports, 2015, 16(8): 975-985.
Atashrazm F, Ellis S. The polarity protein PARD3 and cancer. Oncogene, 2021, 40(25): 4245-4262.

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