Evidence map›Paper›PMID 42377777›Full record

ArticleMolecular biology reports2026

Integrated analysis of UGT1A1 promoter polymorphism, gene expression, and IL-1β reveals genotype-driven susceptibility in Gilbert syndrome.

Sahar M Hussein, Roya Hadi Al-Haddad, Saja Ali Shareef, Mays Talib Abdallah

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1 · What the graph read from it

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Sahar M HusseinDepartment of Molecular and Medical Biotechnology, College of biotechnology, Al-Nahrain University, Baghdad, Iraq. saharhadad84@gmail.com.
Roya Hadi Al-HaddadScientific Research Commission, Baghdad, Iraq. royaalhadad84@gmail.com.
Saja Ali ShareefDepartment of Molecular and Medical Biotechnology, College of biotechnology, Al-Nahrain University, Baghdad, Iraq.
Mays Talib AbdallahDepartment of Molecular and Medical Biotechnology, College of biotechnology, Al-Nahrain University, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGilbert syndrome (GS) is an inherited disorder characterized by unconjugated hyperbilirubinemia as a result of the reduced transcriptional activity of proteins of UGT1A1. The roles and mechanisms of promoter polymorphism, gene expression, and inflammation are not fully understood, particularly in Middle Eastern populations, including Iraq.

methodsA case-control study with 50 GS patients and 50 healthy controls was conducted for identifying the UGT1A1 rs8175347 polymorphism using PCR and Sanger sequencing. RT-qPCR was used to evaluate gene expression, whereas ELISA was used to detect IL-1β levels. Multiple inheritance models were applied to assess genetic association, and regression analyses were used to identify independent predictors.

resultGS patients demonstrated much more prevalently expanded TA-repeat alleles (TA

conclusionUGT1A1 promoter polymorphism appears to be strongly associated with GS susceptibility and transcriptional downregulation, whereas IL-1β may reflect a secondary, non-regulatory inflammatory response.

Indexed as

Gilbert DiseaseGlucuronosyltransferaseInterleukin-1betaAdolescentAdultAllelesCase-Control StudiesFemaleGene ExpressionGenetic Predisposition to DiseaseGenotypeHumansIraqMalePolymorphism, GeneticPolymorphism, Single NucleotideGlucuronosyltransferaseIL1B protein, humanInterleukin-1betaUGT1A1 EnzymeGene expressionGilbert syndromeIL-1βTA-repeat polymorphismUGT1A1

Identifiers

PMID42377777

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