J
Joshua T. Mendell
Researcher at University of Texas Southwestern Medical Center
Publications - 118
Citations - 38826
Joshua T. Mendell is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: microRNA & Regulation of gene expression. The author has an hindex of 54, co-authored 107 publications receiving 32627 citations. Previous affiliations of Joshua T. Mendell include Ohio State University & Johns Hopkins University School of Medicine.
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Journal ArticleDOI
StringTie enables improved reconstruction of a transcriptome from RNA-seq reads
Mihaela Pertea,Geo Pertea,Corina Antonescu,Tsung Cheng Chang,Joshua T. Mendell,Steven L. Salzberg +5 more
TL;DR: StringTie, a computational method that applies a network flow algorithm originally developed in optimization theory, together with optional de novo assembly, to assemble these complex data sets into transcripts produces more complete and accurate reconstructions of genes and better estimates of expression levels.
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c-Myc-regulated microRNAs modulate E2F1 expression.
TL;DR: A mechanism through which c-Myc simultaneously activates E2F1 transcription and limits its translation, allowing a tightly controlled proliferative signal is revealed.
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Functional Classification and Experimental Dissection of Long Noncoding RNAs
Florian Kopp,Joshua T. Mendell +1 more
TL;DR: This review categorizes lncRNA loci into those that regulate gene expression in cis versus those that perform functions in trans and proposes an experimental approach to dissect lncRNAs activity based on these classifications.
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Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis
Tsung Cheng Chang,Erik A. Wentzel,Oliver A. Kent,Kalyani Ramachandran,Michael Mullendore,Kwang Hyuck Lee,Georg Feldmann,Munekazu Yamakuchi,Marcella Ferlito,Charles J. Lowenstein,Dan E. Arking,Michael A. Beer,Anirban Maitra,Joshua T. Mendell +13 more
TL;DR: It is demonstrated that microRNAs (miRNAs) are important components of the p53 transcriptional network and miR-34a-responsive genes are highly enriched for those that regulate cell-cycle progression, apoptosis, DNA repair, and angiogenesis.
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c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism.
Ping Gao,Irina Tchernyshyov,Tsung Cheng Chang,Yun-Sil Lee,Kayoko Kita,Takafumi Ochi,Karen I. Zeller,Angelo M. De Marzo,Jennifer E. Van Eyk,Joshua T. Mendell,Chi V. Dang +10 more
TL;DR: In this paper, the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells.