A partial cDNA for 6-phosphogluconate dehydrogenase (PGD, EC 1.1.1.44) was isolated from a porcine liver cDNA library using a rat PGD cDNA. The identity of the PGD cDNA was confirmed by DNA sequencing and comparison of the amino acid sequence with the corresponding ovine sequence. The PGD cDNA was assigned to 6q2.5-2.7 by in situ hybridization.
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Single-molecule polyadenylated tail sequencing (SM-PAT-Seq) to measure polyA tail lengths transcriptome-wide.
Methods Enzymol
July 2021
Intramural Research Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, United States. Electronic address:
Polyadenylation of the 3' end of mRNAs is an important mechanism for regulating their stability and translation. We developed a nucleotide-resolution, transcriptome-wide, single-molecule SM-PAT-Seq method to accurately measure the polyA tail lengths of individual transcripts using long-read sequencing. The method generates cDNA using a double stranded splint adaptor targeting the far 3' end of the polyA tail for first strand synthesis along with random hexamers for second strand synthesis.
View Article and Find Full Text PDFFMR6 may play a role in the pathogenesis of fragile X-associated premature ovarian insufficiency.
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January 2017
a IVF Unit, Department of Obstetrics and Gynecology , Chaim Sheba Medical Center, (Tel Hashomer) , Ramat Gan , Israel and.
The aim of this study was to evaluate whether long noncoding RNA accumulation play a role in the pathophysiology of fragile X-associated premature ovarian insufficiency (FXPOI). The study population consisted of 22 consecutive fragile X mental retardation 1 (FMR1) premutation carriers (CGGn 55-199 repeats) undergoing in vitro fertilization and pre-implantation genetic diagnosis (IVF-PGD) treatment. The control group consists of 11 patients, with <55 CGG repeats, undergoing IVF-ICSI for male factor infertility, matched by age, treated in the same period.
View Article and Find Full Text PDFChromosome fragility at FRAXA in human cleavage stage embryos at risk for fragile X syndrome.
Am J Med Genet A
October 2015
Centre for Medical Genetics, Universitair Ziekenhuis Brussel (UZ Brussel), Vrije Universiteit Brussel (VUB), Brussel, België
Fragile X syndrome (FXS), the most common inherited intellectual disability syndrome, is caused by expansion and hypermethylation of the CGG repeat in the 5' UTR of the FMR1 gene. This expanded repeat, also known as the rare fragile site FRAXA, causes X chromosome fragility in cultured cells from patients but only when induced by perturbing pyrimidine synthesis. We performed preimplantation genetic diagnosis (PGD) on 595 blastomeres biopsied from 442 cleavage stage embryos at risk for FXS using short tandem repeat (STR) markers.
View Article and Find Full Text PDFDNA repair signalling pathway genes are overexpressed in poor-quality pre-implantation human embryos with complex aneuploidy.
Eur J Obstet Gynecol Reprod Biol
April 2014
Department of Embryology at Reproductive Biomedicine Research Centre, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
Objective: Chromosomal abnormalities and poor quality are correlated with DNA damage in the pre-implantation stage in humans. This study aimed to explore the altered expression of DNA damage signalling pathways - including apoptosis, cell cycle and DNA repair pathways - in poor-quality pre-implantation human embryos with complex aneuploidy.
Study Design: Surplus Day 4 embryos from candidates undergoing pre-implantation genetic screening were pooled into two groups.
In vitro and molecular modeling analysis of two mutant desert hedgehog proteins associated with 46,XY gonadal dysgenesis.
DNA Cell Biol
September 2013
División de Investigación Biomédica, Subdirección de Enseñanza e Investigación, Centro Médico Nacional 20 de Noviembre, Instituto de Seguridad y Servicios Sociales de los Trabajadores del Estado, México, D.F., México.
Mutations of Desert hedgehog (DHH) have been associated to 46,XY pure gonadal dysgenesis (PGD) and to mixed gonadal dysgenesis (MGD); however, there have been no functional studies of mutations described in DHH. To determine if mutations p.L162P and Δ1086delG yield functional impairment, we performed in vitro and in silico analysis of both DHH mutants.
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