Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolation and cloning of abundant reverse transcriptase-polymerase chain reaction (RT-PCR) products from the filarial nematode Brugia malayi using the conserved nematode spliced leader sequence and poly A as amplification targets has allowed us to identify abundant, stage specific transcripts from infective and post-infective larvae. The predicted protein products of the most prominent full-length transcripts from mosquito-derived L3 parasites are: (i) Bm-ALT-1, a homologue of a Dirofilaria immitis abundant larval protein: (ii) Bm-CPI-1, a cystatin-type cysteine protease inhibitor; (iii) Bm-ALT-3, a novel predicted 6 kDa glycine/tyrosine-rich protein; and (iv) Bm-TPH-1, a homologue of a mammalian translationally-controlled tumour protein. Some transcripts were not full-length but had mis-primed at A-rich stretches of coding sequence: the most abundant of these was Bm-col-3, a which encodes a collagen homologous to Bp-COL-1 of Brugia pahangi. Similar analysis of abundant spliced leader (SL)/oligo-dT products from fourth-stage larvae 9 days post-infection yielded two dominant transcripts: (i) Bm-cdd-1, which encodes a protein with homology to cytidine deaminase, differing at only one amino acid position from its homologue described in Brugia pahangi; and (ii) the same truncated form of Bm-col-3 found in L3 preparations. Expression of the major transcripts was assessed by PCR amplification of cDNA libraries derived from each stage of the life cycle. alt1, alt-3 and cpi-1 were all found to be specific to the L3 stage, while cdd-1 was found only in the L4 cDNA library. Expression of these larval-specific transcripts was not detected in either microfilarial or adult libraries.
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PMID:Differentially expressed, abundant trans-spliced cDNAs from larval Brugia malayi. 923 76

TBX22 belongs to the T-box family of transcription factors and was originally found in an in silico approach designed to identify new genes on the human Xq12-q21 region. Mutations in TBX22 have been reported in families with X-linked cleft palate and ankyloglossia (CPX), but the underlying pathogenetic mechanism remained unknown. We have identified mouse Tbx22 and analyzed its expression during embryogenesis by reverse transcriptase-polymerase chain reaction and in situ hybridization. In mouse embryos, it is expressed in distinct areas of the head, namely the mesenchyme of the inferior nasal septum, the posterior palatal shelf before fusion, the attachment of the tongue, and mesenchymal cells surrounding the eye anlage. The localization in the tongue frenulum perfectly correlates with the ankyloglossia phenotype in CPX. Furthermore, we identified positionally conserved binding sites for transcription factors, two of which have been implicated previously in palatogenesis (MSX1, PRX2).
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PMID:Expression of mouse Tbx22 supports its role in palatogenesis and glossogenesis. 1266 95

The molecular regulation of palatogenesis continues to be an active area of investigation to provide a foundation for understanding the molecular etiology of cleft palate. Transforming growth factor (TGF) -beta type III receptor (TbetaR-III) has been shown to be specifically expressed in the medial edge epithelium at critical stages of palatal shelf adherence during palatogenesis. The aim of this study was to examine TbetaR-III mRNA localization and expression levels in vivo and to determine the requirement for TbetaR-III expression during palatal fusion in vitro. TbetaR-III gene expression was analyzed by in situ hybridization in tissue specimens and real-time reverse transcriptase-polymerase chain reaction using specific cells in the palatal shelf isolated by laser capture microdissection. TbetaR-III was knocked down in embryonic day (E) 13 palatal shelves in organ culture. Palatal shelf organ cultures were treated with small interfering RNA (siRNA) at final concentrations of 300, 400, and 500 nM, respectively. The treatment with siRNA specific for TbetaR-III decreased the amount of protein by approximately 75%. The reduction in TbetaR-III resulted in a delay in the process of palatal fusion compared with control. The protein expression of phospho-Smad2 was decreased in the TbetaR-III siRNA group. In addition, palatal organ cultures treated with TbetaR-III siRNA + rhTGF-beta3 completely fused by 72 hr in vitro. These results support our hypothesis that TbetaR-III has a critical role in the process of palatal fusion.
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PMID:Functional role of transforming growth factor-beta type III receptor during palatal fusion. 1729 10

DNA methylation epigenetically regulates gene expression. This study is aimed to investigate genome-wide DNA methylations involved in the regulation of palatal fusion in the all-trans retinoic acid-induced mouse cleft palate model. There were 4,718,556 differentially CCGG methylated sites and 367,504 CCWGG methylated sites for 1497 genes between case and control embryonic mouse palatal tissues. The enhancers (HDAC4 and SMAD3) and promoter (MID1) of these three genes had cis-acting element methylation. HDAC4 is localized within the CCWGG, while MID1 and SMAD3 are localized within the CCGG of the gene intron. The methylation-specific polymerase chain reaction data confirmed the MethylRAD-seq results, while the quantitative reverse transcriptase-polymerase chain reaction result showed that changes in gene expression inversely were associated with the cis-acting element methylation of the gene during retinoic acid-induced palatal fusion. The GO and KEGG data showed that these three genes could regulate cell proliferation, skeletal muscle fiber development, and development-related gene signaling or activity. The cis-acting element methylation of HDAC4, SMAD3, and MID1 may play a regulatory role during palatal fusion. Further research is needed to verify these novel epigenetic biomarkers for cleft palate.
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PMID:Genome-Wide DNA Methylation Profile of Gene cis-Acting Element Methylations in All-trans Retinoic Acid-Induced Mouse Cleft Palate. 3027 13