Hossein Najmabadi

Kariminejad & Najmabadi Pathology and Genetics Center, Teheran, Tehrān, Iran

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Publications (217)677.52 Total impact

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    ABSTRACT: Copy number variations in α-globin genes are results of unequal crossover between homologous segments in the α-globin gene cluster that misalign during the meiosis phase of the gametogenesis process. Reduction or augmentation of α-globin genes leads to imbalance of α/β chains in hemoglobin tetramer and consequently attenuate or worsen the β-thal clinical symptoms, respectively. Multiplications in α-globin genes have been found in some populations, justifying unexpected severe phenotype of β-thal carriers. Unexpected severe phenotype in the family members may result from coexistence of extra α-globin genes, which is an important factor in the causation of thalassemia intermedia and major in heterozygous β-thalassemia. We described different multiplications in α-globin locus in an Iranian family with one, two or three extra α-globin genes (ααα/αα, αααα/αα and αααα/ααα). The excess α-globin gene/genes cause increment in β/α chain imbalance and leads to worsening pathophysiology and clinical severity of β-thalassemia carriers.
    Expert Review of Hematology 08/2015; · 2.14 Impact Factor
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    ABSTRACT: We describe a case of Hb H disease associated with homozygosity for a two nucleotide deletion in the polyadenylation signal of the α2-globin gene (HBA2: c.*93_*94delAA). The patient, a 27-year-old son of a consanguineous couple, needs regular blood transfusions every 6 months.
    Hemoglobin 07/2015; DOI:10.3109/03630269.2015.1059850 · 0.96 Impact Factor
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    ABSTRACT: AIMP1/p43 is a multifunctional non-catalytic component of the multisynthetase complex. The complex consists of nine catalytic and three non-catalytic proteins, which catalyze the ligation of amino acids to their cognate tRNA isoacceptors for use in protein translation. To date, two allelic variants in the AIMP1 gene have been reported as the underlying cause of autosomal recessive primary neurodegenerative disorder. Here, we present two consanguineous families from Pakistan and Iran, presenting with moderate to severe intellectual disability, global developmental delay, and speech impairment without neurodegeneration. By the combination of homozygosity mapping and next generation sequencing, we identified two homozygous missense variants, p.(Gly299Arg) and p.(Val176Gly), in the gene AIMP1 that co-segregated with the phenotype in the respective families. Molecular modeling of the variants revealed deleterious effects on the protein structure that are predicted to result in reduced AIMP1 function. Our findings indicate that the clinical spectrum for AIMP1 defects is broader than witnessed so far.European Journal of Human Genetics advance online publication, 15 July 2015; doi:10.1038/ejhg.2015.148.
    European Journal of HumanGenetics 07/2015; DOI:10.1038/ejhg.2015.148 · 4.23 Impact Factor
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    ABSTRACT: Histamine acts as a neurotransmitter in the brain which participates in the regulation of many biological processes including inflammation, gastric acid secretion, and neuromodulation. The enzyme histamine N-methyltransferase (HNMT) inactivates histamine by transferring a methyl group from S-adenosyl-L-methionine to histamine, and is the only well-known pathway for termination of neurotransmission actions of histamine in mammalian CNS. We performed autozygosity mapping followed by targeted exome sequencing and identified two homozygous HNMT alterations, p.Gly60Asp and p.Leu208Pro in patients affected with nonsyndromic autosomal recessive intellectual disability (NS-ARID) from two unrelated consanguineous families of Turkish and Kurdish ancestry, respectively. We verified the complete absence of a functional HNMT in patients using in vitro toxicology assay. Using mutant and wild type (WT) DNA constructs as well as in silico protein modelling, we confirmed that p.Gly60Asp disrupts the enzymatic activity of the protein, and that p.Leu208Pro results in reduced protein stability, resulting in decreased histamine inactivation. Our results highlight the importance of inclusion of HNMT for genetic testing of individuals presenting with ID. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Human Molecular Genetics 07/2015; DOI:10.1093/hmg/ddv286 · 6.68 Impact Factor
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    ABSTRACT: The 3.7 kb triplicated α-globin gene (ααα(anti 3.7)) mutation has been found in most populations. It results from an unequal crossover between misaligned homologous segments in the α-globin gene cluster during meiosis. The pathophysiology and clinical severity of β-thalassemia (β-thal) are associated with the degree of α chain imbalance. The excess of α-globin chains plays an important role in the pathophysiology of β-thal. When heterozygous/homozygous β-thal coexists with an α gene numerical alteration, the clinical and hematological phenotype of thalassemia could change to mild anemia in case of an α deletion (-α/αα) or severe anemia in the case of an α triplication (αα/ααα). The coexistence of an ααα(anti 3.7) triplication is considered an important factor in the severity of β-thal, exacerbating the phenotypic severity of β-thal by causing more globin chain imbalance. This study shows that the ααα(anti 3.7) triplication is an important factor in the causation of β-thal intermedia (β-TI) in heterozygous β-thal. This type of phenotype modification has rarely been observed and reported in the Iranian population. Here we report the coinheritance of a triplicated α-globin gene arrangement and heterozygous/homozygous β-thal in 23 cases, presenting with a β-TI or β-thal major (β-TM) phenotype. Some of these patients were considered to have a mild β-TI phenotype as they needed no blood transfusions; some occasionally received blood transfusions in their lifetime (for example on delivery) but some are dependent on regular blood transfusions (every 20 to 40 days). Our study was focused on the importance of detecting the α-globin gene triplication in genotype/phenotype prediction in Iranian thalassemia patients.
    Hemoglobin 06/2015; 39(3):1-6. DOI:10.3109/03630269.2015.1027914 · 0.96 Impact Factor
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    ABSTRACT: To analyze the association between TREM2 exon 2 variants and late-onset (sporadic) Alzheimer's disease (AD) in an elderly Iranian population. Exon 2 of TREM2 in a total of 131 AD patients and 157 controls was genotyped using polymerase chain reaction and Sanger sequencing. Fisher's exact test was used to compare the allele and genotype frequency between the 2 study groups. One homozygous and 2 heterozygous carriers of rs75932628-T in the AD patients and 1 heterozygous carrier in the control group were identified. One novel damaging variant, G55R, was also detected in the AD patient group. The frequency of rs75932628-T as well as the amount of rare variants were higher in the AD patients than in the controls, but this did not reach a statistically significant association with AD (odds ratio: 4.8; 95% confidence interval: 0.54 to 43.6; p = 0.270). The rs75932628-T allele frequency in the elderly Iranian population (0.86%) was high. © 2015 S. Karger AG, Basel.
    Medical Principles and Practice 05/2015; 24(4). DOI:10.1159/000430842 · 1.11 Impact Factor
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    ABSTRACT: α-Thalassemia (α-thal) is a common genetic disorder in Iran and many parts of the world. Genetic defects in the α-globin gene cluster can result in α-thal that may develop into a clinical phenotype varying from almost asymptomatic to a lethal hemolytic anemia. Loss of one functional α gene, indicated as heterozygous α(+)-thal, shows minor hematological abnormalities. Homozygosity for α(+)- or heterozygosity for α(0)-thal have more severe hematological abnormalities due to a markedly reduced α chain output. At the molecular level, the absence of three α-globin genes resulting from the compound heterozygous state for α(0)- and α(+)-thal, lead to Hb H disease. Here we present a 21 nucleotide (nt) duplication consisting of six amino acids and 3 bp of intronic sequence at the exon-intron boundary, in both the α-globin genes, detected by direct DNA sequencing. This duplication was identified in three patients originating from two different Iranian ethnic groups and one Arab during more than 12 years. The clinical presentation of these individuals varies widely from a mild asymptomatic anemia (heterozygote in α1-globin gene) to a severely anemic state, diagnosed as an Hb H individual requiring blood transfusion (duplication on the α2-globin gene in combination with the - -(MED) double α-globin gene deletion). The third individual, who was homozygous for this nt duplication on the α1-globin gene, showed severe hypochromic microcytic anemia and splenomegaly. In the last decade, numerous α-globin mutations have demonstrated the necessity of prenatal diagnosis (PND) for α-thal, and this study has contributed another mutation as important enough that needs to be considered.
    Hemoglobin 05/2015; 39(3):1-5. DOI:10.3109/03630269.2015.1030757 · 0.96 Impact Factor
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    ABSTRACT: We have investigated the efficacy of QF-PCR for the prenatal recognition of common aneuploidy and compared our findings with cytogenetic results in our laboratories. A total of 4058 prenatal samples (4031 amniotic fluid and 27 chorionic villous samples) were analyzed by QF-PCR using several selected STR markers together with amelogenin. Results were compared to those obtained by conventional cytogenetic analysis. We detected 139 (3.42%) numerical abnormalities in our subjects by QF-PCR. Concordant QF-PCR and karyotype results were obtained in 4001 (98.59%) of the samples. An abnormal karyotype associated with adverse clinical outcome undetected by QF-PCR was found in 16.66% (n = 28) of samples. Using QF-PCR alone, we were able to detect abnormalities in 98.59% of all referred families; however the karyotyping results improved the detection rate to 99.85% of the referred cases. Individuals with neonatal screening result with 1:10 risk ratio showed 11.29% abnormal karyotype while this number was 2.16% in mothers with risk ratio of 1:250 or less. In countries where large scale conventional cytogenetic is hampered by its high cost and lack of technical expertise, QF-PCR may be used as the first line of screening for detection of chromosomal abnormalities. We also recommend QF-PCR for all the families that are seeking prenatal diagnosis of single gene disorders aneuploidies screening to be added to their work up.
    05/2015; 18(5):296-303.
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    ABSTRACT: Congenital cardiac and neurodevelopmental deficits have been recently linked to the mediator complex subunit 13-like protein MED13L, a subunit of the CDK8-associated mediator complex that functions in transcriptional regulation through DNA-binding transcription factors and RNA polymerase II. Heterozygous MED13L variants cause transposition of the great arteries and intellectual disability (ID). Here, we report eight patients with predominantly novel MED13L variants who lack such complex congenital heart malformations. Rather, they depict a syndromic form of ID characterized by facial dysmorphism, ID, speech impairment, motor developmental delay with muscular hypotonia and behavioral difficulties. We thereby define a novel syndrome and significantly broaden the clinical spectrum associated with MED13L variants. A prominent feature of the MED13L neurocognitive presentation is profound language impairment, often in combination with articulatory deficits.European Journal of Human Genetics advance online publication, 11 March 2015; doi:10.1038/ejhg.2015.26.
    European journal of human genetics: EJHG 03/2015; DOI:10.1038/ejhg.2015.26 · 4.23 Impact Factor
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    ABSTRACT: Knowledge of the genes responsible for intellectual disability, particularly autosomal recessive forms, is rapidly expanding. Increasing numbers of the gene show great heterogeneity and supports the hypothesis that human genome may contain over 2000 causative genes with a critical role in brain development. Since 2004, we have applied genome-wide SNP genotyping and next-generation sequencing in large consanguineous Iranian families with intellectual disability, to identify the genes harboring disease-causing mutations. The current study paved the way for identification of responsible genes in two unrelated Iranian families. We found two novel nonsense mutations, p.C77* and p.Q115*, in the calpain catalytic domain of CAPN10, which is a cysteine protease known to be involved in pathogenesis of noninsulin-dependent diabetes mellitus. Another different mutation in this gene (p.S138_R139ins5) has previously been reported in an Iranian family. All of these patients have common clinical features in spite of specific brain structural abnormalities on MRI. Different mutations in CAPN10 have already been found in three independent Iranian families. These results have strongly supported the possible role of CAPN10 in human brain development. Altogether, we proposed CAPN10 as a promising candidate gene for intellectual disability, which should be considered in diagnostic gene panels.
    Archives of Iranian medicine 03/2015; 18(3):179-84. · 1.11 Impact Factor
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    ABSTRACT: We report on Dutch and Iranian families with affected individuals who present with moderate to severe intellectual disability and additional phenotypes including progressive tremor, speech impairment, and behavioral problems in certain individuals. A combination of exome sequencing and homozygosity mapping revealed homozygous mutations c.484G>A (p.Gly162Arg) and c.1898C>G (p.Pro633Arg) in SLC6A17. SLC6A17 is predominantly expressed in the brain, encodes a synaptic vesicular transporter of neutral amino acids and glutamate, and plays an important role in the regulation of glutamatergic synapses. Prediction programs and 3D modeling suggest that the identified mutations are deleterious to protein function. To directly test the functional consequences, we investigated the neuronal subcellular localization of overexpressed wild-type and mutant variants in mouse primary hippocampal neuronal cells. Wild-type protein was present in soma, axons, dendrites, and dendritic spines. p.Pro633Arg altered SLC6A17 was found in soma and proximal dendrites but did not reach spines. p.Gly162Arg altered SLC6A17 showed a normal subcellular distribution but was associated with an abnormal neuronal morphology mainly characterized by the loss of dendritic spines. In summary, our genetic findings implicate homozygous SLC6A17 mutations in autosomal-recessive intellectual disability, and their pathogenic role is strengthened by genetic evidence and in silico and in vitro functional analyses. Copyright © 2015 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.
    The American Journal of Human Genetics 02/2015; 96(3). DOI:10.1016/j.ajhg.2015.01.010 · 10.99 Impact Factor
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    ABSTRACT: Background: Age-related macular degeneration (AMD) is a complex disorder which results in irreversible vision loss and progressive impairment of central vision. Disease susceptibility is influenced by multiple genetic and environmental factors. Single nucleotide polymorphisms (SNP) in the complement factor H gene are the most important genetic risk factors. We conducted a case-control study to investigate the association four SNPs (dbSNP ID: rs800292, rs1061170, rs2274700 and rs3753395) of CFH gene with AMD in the Iranian population. Materials and Methods: We recruited 100 AMD patients and 100 age- and sex-matched normal controls. Direct sequencing for three SNPs (rs800292, rs2274700 and rs3753395) and restriction fragment length polymorphism utilized for rs1061170. Allele and genotype frequencies of SNPs were calculated and tested for departure from Hardy–Weinberg equilibrium using the Chi-square test. An allelic and genotypic association was compared by logistic regression analysis using the SNPassoc. Results: According to our results, the frequencies of risk allele for all SNPs (G, G, A, and C alleles of rs800292, rs2274700, rs3753395 and rs1061170, respectively) were significantly higher in AMD patients (p value < 0.001). AMD individuals who had at least one copy of the C allele of rs1061170 had an increased risk of disease compared with cases with the T allele. Other studied polymorphisms showed the same association. Conclusion: Our results suggest the contribution of all four predicted CFH polymorphisms in AMD susceptibility among the Iranian population. This association with CFH may lead to early detection and new strategies for prevention and treatment of AMD.
    Ophthalmic Genetics 01/2015; DOI:10.3109/13816810.2014.955585 · 1.23 Impact Factor
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    ABSTRACT: The Krüppel-like factor 1 (KLF1) is an essential erythroid-specific transcription factor. Mutations in the human KLF1 gene have different phenotypic effects, ranging from increased Hb F levels to the disruption of erythropoiesis. Here, we screened 227 Iranian β-thalassemia (β-thal) patients for the presence of KLF1 mutations by using the single-strand conformational polymorphism (SSCP) approach. Our aim was to assess the potential effect of these mutations on the β-thal disease severity. After screening, two variants were found. One patient carried a potentially deleterious variant (Polyphen-2) in exon 2 (p.F182L). Another patient was homozygous for a previously unreported intronic variant (KLF1: c.911 + 84A > G). The patient with the p.F182L variant (KLF1: c.544T > C) had noticeably high Hb A2 levels (7.6%), consistent with the phenotypic effect of several previously characterized KLF1 mutations in the same exonic region. In addition, he had higher platelet counts (1,069,000/μL) compared to other patients in the cohort.
    Hemoglobin 01/2015; 39(1). DOI:10.3109/03630269.2014.991023 · 0.96 Impact Factor
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    ABSTRACT: Mutations in plectin, a widely expressed giant cytolinker protein can lead to different diseases mostly with signs of muscular dystrophy (MD) and skin blistering. The only report of plectin-related disease without skin involvement is limb-girdle muscular dystrophy type 2Q (LGMD2Q) phenotype, showing early-onset limb-girdle muscular dystrophy symptoms with progressive manner and no cranial muscle involvement. Here, we report a non-consanguineous Iranian family with two affected sisters showing progressive limb and ocular muscle weakness. Whole Exome Sequencing (WES) led to identification of a compound heterozygous mutations, p.Gln1022Ter (c.3064C>T) and p.Gly3835Ser (c.11503G>A), in PLEC gene. To the best of our knowledge, this would be the first report of a patient with LGMD and myasthenic symptoms without any skin involvement, caused by plectinopathy. This observation extends the phenotypic spectrum of PLEC related diseases and suggests a variable expression of the PLEC- related symptoms.
    Archives of Iranian medicine 01/2015; 18(1):60-4. · 1.11 Impact Factor
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    ABSTRACT: Hereditary hearing loss is the most common neurosensory disorder in humans. Half of the cases have genetic etiology with extraordinary genetic heterogeneity. Mutations in one gene, GJB2, are the most common cause for autosomal recessive non-syndromic hearing loss (ARNSHL) in many different populations. GJB2 encodes a gap junction channel protein (connexin 26), and is located on DFNB1 locus on chromosome 13q12.11 which also involve another connexin gene, GJB6. Mutation screening of GJB2 revealed that a high number of patients with deaf phenotype have heterozygous genotype and carry only one mutant allele. As the first comprehensive study in Iran, we have targeted GJB2-related Iranian heterozygotes, looking for second mutant allele which leads to hearing impairment. They bear first mutation in their coding exon of GJB2. Using PCR-based direct sequencing, we assessed 103 patients with ARNSHL for variants in non-coding exon and promoter region of this gene, for the first time in Iran. We have identified the second mutant allele in splice site of exon-1 of GJB2 which is known as IVS1+1G>A in 17 probands. We found no mutation in promoter region of GJB2. Our findings reveal that IVS1+1G>A mutation in noncoding exon of GJB2 is the most common mutation after 35delG within multi ethnical Iranian heterozygote samples. It emphasizes to approach exon1 of GJB2 in case of ARNSHL genetic diagnosis. Copyright © 2014. Published by Elsevier Ireland Ltd.
    International Journal of Pediatric Otorhinolaryngology 12/2014; 79(2). DOI:10.1016/j.ijporl.2014.11.024 · 1.32 Impact Factor
  • F Zeinali · M Mohseni · M Fadaee · Z Fattahi · H Najmabadi · H Otukesh · K Kahrizi
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    ABSTRACT: Hearing defects are the most common sensory disorders, affecting 1 out of every 500 newborns. ATP6V1B mutations are associated with early sensorineural hearing loss, whereas ATP6V0A4 mutations are classically associated with either late-onset sensorineural hearing loss or normal hearing. ATP6V1B1 and ATP6V0A4 genetic mutations cause recessive forms of distal renal tubular acidosis. Ten unrelated deaf Iranian families with distal renal tubular acidosis were referred to the Genetics Research Centre, University of Social Welfare and Rehabilitation Sciences, Tehran. All exons of the ATP6V1B1 and ATP6V0A4 genes were sequenced in affected family members. We identified a previously reported ATP6V1B1 frameshift mutation (P385fsX441) in two families and a nucleotide substitution in exon 10 (P346R) in three families. In addition, one patient was homozygous for a novel nucleotide substitution in exon 3. ATP6V1B1 genetic mutations were detected in more than half of the families studied. Mutations in this gene therefore seem to be the most common causative factors in hearing loss associated with distal renal tubular acidosis in these families.
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    ABSTRACT: Next-generation sequencing has greatly accelerated the search for disease-causing defects, but even for experts the data analysis can be a major challenge. To facilitate the data processing in a clinical setting, we have developed a novel Medical Re-sequencing Analysis Pipeline (MERAP). MERAP assesses the quality of sequencing, and has optimized capacity for calling variants, including Single Nucleotide Variants, insertions and deletions, Copy Number Variation, and other structural variants. MERAP identifies polymorphic and known causal variants by filtering against public-domain databases, and flags non-synonymous and splice-site changes. MERAP uses a logistic model to estimate the causal likelihood of a given missense variant. MERAP considers the relevant information such as phenotype and interaction with known disease-causing genes. MERAP compares favorably with GATK, one of the widely used tools, because of its higher sensitivity for detecting indels, its easy installation, and its economical use of computational resources. Upon testing more than 1200 individuals with mutations in known and novel disease genes, MERAP proved highly reliable, as illustrated here for 5 families with disease-causing variants. We believe that the clinical implementation of MERAP will expedite the diagnostic process of many disease-causing defects.This article is protected by copyright. All rights reserved
    Human Mutation 12/2014; 35(12). DOI:10.1002/humu.22695 · 5.05 Impact Factor
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    ABSTRACT: Chromosome instability is the most common form of genomic instability. Genomic instability can lead to tumorogenesis. High level of chromosomal aberrations in peripheral blood lymphocytes can be used as a biomarker for cancer. Air pollution is one of the most important factors that cause chromosomal instability (CIN). In this comparative study we used classic Cytogenetic technique to analyze the effects of air pollutants on chromosome stability. We collected peripheral blood from 30 taxi drivers of two polluted districts (districts 6 and 7) in Tehran and 30 taxi drivers from rural areas of Lahijan, north of Iran. Comparison of the level of chromosome breakage in the two groups showed an increased level of chromosome breakage in the drivers from polluted districts of Tehran, although not significant, using Fisher exact test (p-value = 0.300). However, the overall chromosome aberration rate (including both chromosome and chromatid gaps), the difference was significant using Chi-square test (p-value = 0.012). An increased level of chromosome aberration was present in the drivers from polluted districts of Tehran compared to drivers from non-polluted areas in Lahijan.
    Journal of Environmental Health Science and Engineering 12/2014; 12(1):144. DOI:10.1186/s40201-014-0144-0 · 1.01 Impact Factor
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    ABSTRACT: IntroductionUsher syndrome (USH) is an autosomal recessive disease characterized by bilateral sensorineural hearing impairment (ARSNHL), and progressive visual loss due to retinitis pigmentosa (RP) with the present or absent of vestibular dysfunction. USH is classified into three types based on the severity and progression of the clinical periods of the disease. Usher syndrome type 1 (USH1) which is manifested by severe to profound congenital hearing loss, vestibular dysfunction and prepubertal onset of RP is the most severe form of the USH (Millan et al. 2011; Le Quesne Stabej et al. 2012). Patients with Usher type 2, presented at the second decade of the life, are characterized by moderate to severe hearing loss (HL), normal vestibular function and RP. For Usher type 3 (USH3) clinically, postlingual progressive HL, RP and variable vestibular function are the most distinguished features (Dai et al. 2008; Millan et al. 2011; Le Quesne Stabej et al. 2012). Genetically, USH is highly het ...
    Journal of Genetics 12/2014; 93(3):837-41. DOI:10.1007/s12041-014-0443-3 · 1.01 Impact Factor
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    ABSTRACT: NDST1 was recently proposed as a candidate gene for autosomal recessive intellectual disability in two families. It encodes a bifunctional GlcNAc N-deacetylase/N-sulfotransferase with important functions in heparan sulfate biosynthesis. In mice, Ndst1 is crucial for embryonic development and homozygous null mutations are perinatally lethal. We now report on two additional unrelated families with homozygous missense NDST1 mutations. All mutations described to date predict the substitution of conserved amino acids in the sulfotransferase domain, and mutation modeling predicts drastic alterations in the local protein conformation. Comparing the four families, we noticed significant overlap in the clinical features, including both demonstrated and apparent intellectual disability, muscular hypotonia, epilepsy, and postnatal growth deficiency. Furthermore, in Drosophila, knockdown of sulfateless, the NDST ortholog, impairs long-term memory, highlighting its function in cognition. Our data confirm NDST1 mutations as a cause of autosomal recessive intellectual disability with a distinctive phenotype, and support an important function of NDST1 in human development. © 2014 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 11/2014; 164A(11). DOI:10.1002/ajmg.a.36723 · 2.05 Impact Factor

Publication Stats

3k Citations
677.52 Total Impact Points


  • 2003–2015
    • Kariminejad & Najmabadi Pathology and Genetics Center
      Teheran, Tehrān, Iran
  • 2001–2015
    • University of Social Welfare and Rehabilitation Sciences
      • Genetics Research Center
      Teheran, Tehrān, Iran
  • 2011
    • Quaid-i-Azam University
      • Department of Biochemistry
      Islāmābād, Islāmābād, Pakistan
  • 2009
    • University of Iowa
      • Department of Otolaryngology-Head and Neck Surgery
      Iowa City, IA, United States
  • 2007
    • Max Planck Institute for Molecular Genetics
      • Department of Human Molecular Genetics
      Berlin, Land Berlin, Germany
  • 2004
    • Tehran University of Medical Sciences
      • School of Medicine
      Tehrān, Ostan-e Tehran, Iran