Two-hybrid screening of FAM13A protein partners in lung epithelial cells

Abstract

Objectives: Family with sequence similarity 13 member A (FAM13A) genetic variants have been associated with several chronic respiratory diseases including chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), idiopathic pulmonary fibrosis (IPF) and lung cancer. The FAM13A protein includes a RhoGTPase activating protein (RhoGAP) domain known to participate in various cellular mechanisms including cell proliferation. While intensive genomic studies have been performed to reveal its involvement in lung diseases, the biological role of FAM13A protein is still not completely elucidated. Results: We therefore performed a two-hybrid screening to identify protein partners of FAM13A using a human lung cancer cDNA library. We identified several protein partners with a high confidence score. Researchers in the field of chronic lung diseases may benefit from this two-hybrid screening data which may reveal new research pathways to decipher.

Predictors of lung function trajectories in population‐based studies: A systematic review

“…These phases may be influenced by several modifiable or non‐modifiable adverse exposures leading to lung function deficits and subsequently to chronic obstructive pulmonary disease (COPD) 2–6 . Genetic susceptibility, chronic lung conditions and environmental factors may influence lung function trajectory 1,6–11 . Adverse impacts from preconception, intrauterine and early life exposures may result in lower lung function at birth and/or reduced lung function growth leading to failure to attain maximal peak lung function, while impacts from adult life exposures may result in early or accelerated lung function decline 6 …”

“…[2][3][4][5][6] Genetic susceptibility, chronic lung conditions and environmental factors may influence lung function trajectory. 1,[6][7][8][9][10][11] Adverse impacts from preconception, intrauterine and early life exposures may result in lower lung function at birth and/or reduced lung function growth leading to failure to attain maximal peak lung function, while impacts from adult life exposures may result in early or accelerated lung function decline. 6 Recent evidence shows that failure to attain peak lung function is a risk factor for an early onset of COPD, [1][2][3]12 even if the decline phase is normal.…”

Epigenomic and Transcriptomic Prioritization of Candidate Obesity-Risk Regulatory GWAS SNPs

“…For example, CABLES1 affects CDK5 phosphorylation, which, in turn, controls phosphorylation of the critical adipose-related TF PPARG [51]. FAM13A protein is also implicated in diverse types of signaling [61], including adipocyte insulin signaling [36] and Wnt/beta-catenin signaling, which is crucial for normal development and homeostasis of adipose tissue and other lineages [62,63]. Knockdown of FAM13A during in vitro adipogenesis increases expression of several adipocyte markers [11,14], while in vitro overexpression leads to preadipocyte apoptosis [64].…”

Epigenomic and transcriptomic prioritization of candidate obesity-risk regulatory GWAS SNPs

“…For example, CABLES1 affects CDK5 phosphorylation, which, in turn, controls phosphorylation of the critical adipose-related TF PPARG (52). FAM13A protein is also implicated in diverse types of signaling (62), including adipocyte insulin signaling (32) and Wnt/beta-catenin signaling, which is crucial for normal development and homeostasis of adipose tissue and other lineages (63,64). Knockdown of FAM13A during in vitro adipogenesis increases expression of several adipocyte markers (11,34) while in vitro overexpression leads to preadipocyte apoptosis (65).…”