Evidence map›Paper›PMID 37942259›Full record

ArticleInternational journal of molecular and cellular medicine2023

Mutational Analysis and Genotype Investigation of Less Known Gaucher Mutations through Haplotype Analysis in Iranian Gaucher Patients.

Negar Sardarpour, Hamideh Bagherian, Fatemeh Zafarghandi Motlagh, Tina Shirzadeh, Sadaf Asnavandi, Shahrzad Younesikhah, Shadab Salehpour, Aria Setoodeh, Mohammad Reza Alaei, Sirous Zeinali

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In one paragraph

Article in International journal of molecular and cellular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 38% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 2 citations in OpenAlex.

  1. Pooled it
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  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Negar SardarpourDepartment of Biotechnology, College of Science, University of Tehran, Tehran, Iran.
Hamideh BagherianKawsar Human Genetics Research Center, No. 41 Majlesi St., Vali Asr St, Tehran, Iran.
Fatemeh Zafarghandi MotlaghKawsar Human Genetics Research Center, No. 41 Majlesi St., Vali Asr St, Tehran, Iran.
Tina ShirzadehKawsar Human Genetics Research Center, No. 41 Majlesi St., Vali Asr St, Tehran, Iran.
Sadaf AsnavandiKawsar Human Genetics Research Center, No. 41 Majlesi St., Vali Asr St, Tehran, Iran.
Shahrzad YounesikhahKawsar Human Genetics Research Center, No. 41 Majlesi St., Vali Asr St, Tehran, Iran.
Shadab SalehpourDepartment of Pediatric Endocrinology and Metabolism, Mofid Children's Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Aria SetoodehGrowth and Development Research Center, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
Mohammad Reza AlaeiDepartment of Pediatric Endocrinology and Metabolism, Mofid Children's Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Sirous ZeinaliKawsar Human Genetics Research Center, No. 41 Majlesi St., Vali Asr St, Tehran, Iran.
Shahid Beheshti University of Medical Sciences · IRTehran University of Medical Sciences · IRUniversity of Tehran · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gaucher's disease (GD) is the most frequent lysosomal storage disorder resulting from a deficiency of the enzyme glucocerebrosidase (GBA) which causes the accumulation of glucocerebroside. More than 500 mutations have been reported on the GBA gene so far. In this study, we aimed to investigate more on the genotype of less known mutations through haplotype analysis to explain their disease-causing inheritance. Eight patients and three carriers from nine different families were enrolled in the study. DNA sequencing of all GBA gene's exons was performed and pathogenicity of the mutations was investigated. Using GBA gene-linked STR markers, allele segregations were determined in some families. A total of six different mutations were determined. Five and three patients were identified to carry mutations in homozygous and compound heterozygote patterns respectively, three participants also were identified as carriers. The most prevalent mutations were c.1448 T>C and RecNcil, however, three less common mutations were identified (i.e., c.1223 C>T, c.1315 A>G, and c.1214 G>C). In conclusion, we evaluated six different mutations in Iranian patients and elucidated the inheritance of the three less-known mutations by linkage analysis.

Indexed as

beta-glucocerebrosidaseGaucher diseasehaplotype analysisIranlysosomal storage disorder

Identifiers

PMID37942259
PMCPMC10629722
OpenAlexW4388539972

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.