Robert D. Wells
Texas A&M University
5 Papers
Robert D. Wells is an academic researcher from Texas A&M University. The author has contributed to research in topics: Gene & Frataxin. The author has an hindex of 5, co-authored 5 publications. Previous affiliations of Robert D. Wells include Texas Medical Center.
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Papers
GGA*TCC-interrupted triplets in long GAA*TTC repeats inhibit the formation of triplex and sticky DNA structures, alleviate transcription inhibition, and reduce genetic instabilities.
Naoaki Sakamoto,Jacquelynn E. Larson,Ravi R. Iyer,Laura Montermini,Massimo Pandolfo,Robert D. Wells +5 more
TL;DR: It is proposed that the interruptions introduce base mismatches into the R·R·Y triplex, which explains the observed chemical and biological properties of sticky DNA.
Sticky DNA: self-association properties of long GAA.TTC repeats in R.R.Y triplex structures from Friedreich's ataxia.
Naoaki Sakamoto,Paul D. Chastain,Pawel Parniewski,Keiichi Ohshima,Massimo Pandolfo,Jack D. Griffith,Robert D. Wells +6 more
TL;DR: A novel DNA structure, sticky DNA, is described for lengths of (GAA.TTC)n found in intron 1 of the frataxin gene of Friedreich's ataxia patients and R.R.Y triplexes and/or sticky DNA may be involved in the etiology of FRDA.
A nonpathogenic GAAGGA repeat in the Friedreich gene: implications for pathogenesis.
Keiichi Ohshima,Naoaki Sakamoto,Malgorzata Labuda,John Poirier,Melinda L. Moseley,Laura Montermini,Laura P.W. Ranum,Robert D. Wells,Massimo Pandolfo,Massimo Pandolfo +9 more
TL;DR: It is suggested that such a triplex structure is essential for suppression of gene expression in transfected cells shown by pathogenic GAA repeats of similar length.
Inhibitory effects of expanded GAA.TTC triplet repeats from intron I of the Friedreich ataxia gene on transcription and replication in vivo.
TL;DR: In vivo investigation revealed that expanded GAA·TTC repeats from intron I of the FRDA gene inhibit transcription rather than post-transcriptional RNA processing and also interfere with replication, suggesting the molecular basis for these effects may be the formation of non-B DNA structures.
Sticky DNA, a self-associated complex formed at long GAA*TTC repeats in intron 1 of the frataxin gene, inhibits transcription.
TL;DR: The results suggest that the role of sticky DNA in FRDA may be the sequestration of transcription factors, as well as another DNA molecule used as an internal control in an orientation-independent manner.