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Palmitic acid regulated anti-inflammatory long noncoding RNA (PARAIL)

Target
PARAIL
Molecular classification
Long noncoding RNA (lncRNA)
01

Overview

Palmitic acid regulated anti-inflammatory lncRNA (PARAIL) is a long noncoding RNA induced by palmitic acid, cytokines, and infectious agents in monocytes and macrophages[1]. It is upregulated during the resolution phase of inflammation and functions by interacting with RNA-binding proteins, notably ELAVL1, to modulate the stability and expression of inflammatory genes. Knockdown of PARAIL leads to increased pro-inflammatory gene expression, while overexpression attenuates inflammation. Mouse orthologs of PARAIL are downregulated in diabetic and atherosclerotic conditions, linking its expression to metabolic disease progression[1]. It is also implicated in cancer biology, as high expression correlates with poor prognosis in colorectal cancer and is associated with immune cell infiltration and immune checkpoint gene expression[3][4]. PARAIL represents a novel therapeutic target for diseases driven by chronic inflammation and immune dysregulation[1][3][4].

Other names
AF117829.1RIPK2 divergent transcriptRIPK2-DTPARAIL
02

Mechanism of action

Modulation of PARAIL expression or function Antisense oligonucleotides or lncRNA mimics could theoretically be used to enhance or suppress PARAIL function, influencing pro- or anti-inflammatory gene expression

03

Biological functions

Resolution of inflammationImmune modulationRegulation of inflammatory gene expressionInteraction with RNA-binding proteins (e.g., ELAVL1)Regulation of CD8+ T cell cytotoxic function
04

Disease associations

InflammationCardiometabolic disease (e.g., diabetes, atherosclerosis)Cancer (promotes malignant progression in colorectal cancer)Immune dysregulation
05

Safety considerations

Potential immune suppressionOff-target effects in immune modulation
06

Biomarkers

PARAIL/AF117829.1 expression in monocytes, macrophages, and tumor tissue

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