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Integrator complex subunit 6 (INTS6)

Target
INTS6
Molecular classification
Other (Integrator complex subunit), Enzyme (putative RNA helicase, DEAD box family), Transcription regulator (as part of the integrator complex)
01

Overview

Integrator complex subunit 6 (INTS6) is a component of the multiprotein integrator complex involved in transcriptional regulation by RNA polymerase II, notably 3'-end processing of small nuclear RNAs (snRNAs) and regulatory termination of transcription, including non-coding RNAs such as enhancer RNAs, telomerase RNAs, and long non-coding RNAs[1][7]. INTS6 functions as a molecular adapter that aids in assembly of protein phosphatase 2A (PP2A) subunits to the core complex, facilitating transcription pause-release checkpoint control[1][7]. It is classified as a DEAD-box RNA helicase family member, featuring an Asp-Glu-Ala-Asp (DEAD) motif, with broad roles in gene expression regulation and nucleic acid metabolism[1][5][4]. Additionally, INTS6 promotes DNA repair by homologous recombination and is implicated in maintaining genome integrity[3]. INTS6 is context-dependent in cancer: it acts as a tumor suppressor in hepatocellular and prostate cancers by inhibiting cell proliferation and reducing Wnt/β‐catenin signaling, but may promote tumor growth in colorectal cancer via AKT and ERK pathway activation[3]. No drugs are currently reported to specifically target INTS6, either as inhibitors or activators, and there are no established mechanisms of action, established biomarkers, or safety concerns documented for INTS6-modulating therapies[1][3][5][7].

Other names
DBI1DDX26DDX26AInt6DICE1HDBNotchl2DBI-1protein deleted in cancer 1DEAD box proteinDEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 26RNA helicase HDB
02

Biological functions

RNA processingTranscription regulationmRNA 3'-end processingHomologous recombination and genome integrityCell cycle regulationDNA repair
03

Disease associations

Cancer (tumor suppressor in several cancer types, promoter in others)Other (role in genome integrity maintenance, DNA repair deficiency syndromes)

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