Target intelligence / Profile preview

Zinc finger protein 385A (ZNF385A)

Target
ZNF385A
Molecular classification
Transcription factor, RNA-binding protein, Zinc finger protein
01

Overview

Zinc finger protein 385A (ZNF385A) is a C2H2-type zinc finger protein that functions as a transcription factor and RNA-binding protein. It binds single- and double-stranded RNA and directly interacts with proteins such as PTBP1, TARDBP, and ELAVL1, impacting their function and the regulation of RNA splicing. ZNF385A modulates the cellular response to double-stranded RNA, negatively regulating type-I interferon signaling and maintaining dsRNA homeostasis. In addition, it affects cell cycle progression and apoptosis by interacting with p53/TP53 pathway proteins and regulating their nuclear export and activity. ZNF385A is also implicated in adipogenesis, megakaryocyte differentiation, and disease states such as cancer, where its expression correlates with poor prognosis and may serve as a target for combination immunotherapy. Loss of ZNF385A results in increased interferon response, accumulation of retroelement-derived dsRNA, and enhanced sensitivity to chemotherapeutic agents and NK cell-mediated cytotoxicity, suggesting potential utility in cancer therapies.

Other names
ZNF385AHZFRZFZNF385DKFZp586G1122HzfZFP385Hematopoietic zinc finger proteinRetinal zinc finger proteinzinc finger protein 385
02

Mechanism of action

Modulation of interferon signaling via dsRNA accumulation (by ZNF385A knockout); Enhancement of tumor cell killing by natural killer (NK) cells via increased IFN-I response upon ZNF385A depletion; Facilitation of 5-AZA-CdR efficacy through activation of innate immunity in cancer cells lacking ZNF385A.

03

Biological functions

Regulation of cell cycleRegulation of apoptosisRNA splicingRegulation of interferon signalingRegulation of mRNA localization and translationAdipogenesisRegulation of p53/TP53 signalingMegakaryocyte differentiation
04

Disease associations

CancerEncephalopathy, neonatal severe due to Mecp2 mutationsCone-rod dystrophy 2
05

Safety considerations

Potential induction of autoimmunity or chronic inflammation when inhibited or deleted, due to aberrant interferon response (type-I IFN) and dsRNA accumulationDisruption of RNA splicing and transcript stability
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Interacting drugs

5-Aza-2’-deoxycytidine (5-AZA-CdR)
07

Biomarkers

Overexpression linked to poor prognosis in multiple cancer types (pan-cancer biomarker)

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