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Long intergenic non-coding adipose anti-inflammatory (LINC-ADAIN)

Target
LINC-ADAIN
Molecular classification
Long non-coding RNA (lncRNA), Long intergenic non-coding RNA (lincRNA)
01

Overview

LINC-ADAIN (long intergenic non-coding adipose anti-inflammatory) is a human lincRNA whose expression is reduced in the white adipose tissue of obese individuals. Its depletion increases the stability and translation of KLF5 and IL-8 mRNAs by interacting with IGF2BP2, leading to enhanced adipogenic programs and increased local inflammation, which mirror obesity-induced adipose tissue dysfunction. LINC-ADAIN acts as a suppressor of adipose tissue expansion, lipid storage, and inflammation; thus, it may be important in limiting the development of obesity-related metabolic complications such as insulin resistance, type 2 diabetes, and cardiovascular disease. LINC-ADAIN is part of the emerging class of regulatory RNAs in metabolism, distinct from known protein-coding adipokines. It acts via post-transcriptional regulation of major inflammatory and adipogenesis-related genes (notably KLF5 and IL-8) and directly interacts with the mRNA-binding protein IGF2BP2. No evidence in current literature links LINC-ADAIN to direct drug targeting or pharmaceutical interventions.

Other names
LINC-DMRT2lnc-DMRT2LINC01230TCONS_00015639Linc-ADAIN
02

Biological functions

Regulation of adipogenesis (differentiation of adipose cells)Anti-inflammatory modulation in adipose tissueControl of mRNA stability and translation (via interactions with IGF2BP2)Suppression of adipose tissue expansion and lipid storage
03

Disease associations

ObesityType 2 diabetesCardiovascular disease (via links to adipose tissue dysfunction and inflammation)
04

Biomarkers

Downregulation in obese human white adipose tissue, associated with increased inflammationExpression levels may correlate with adipose tissue health and metabolic disease risk

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