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Mark A. Nelson
University of Arizona
97Publications
32H-index
2,742Citations
Publications 97
Newest
Published on Jul 1, 2019in Neurobiology of Disease5.16
Udaiyappan Janakiraman (UA: University of Arizona), Jie Yu1
Estimated H-index: 1
(ZJNU: Zhejiang Chinese Medical University)
+ 6 AuthorsMark A. Nelson32
Estimated H-index: 32
(UA: University of Arizona)
Abstract TAF1/MRSX33 intellectual disability syndrome is an X-linked disorder caused by loss-of-function mutations in the TAF1 gene. How these mutations cause dysmorphology, hypotonia, intellectual and motor defects is unknown. Mouse models which have embryonically targeted TAF1 have failed, possibly due to TAF1 being essential for viability, preferentially expressed in early brain development, and intolerant of mutation. Novel animal models are valuable tools for understanding neuronal patholog...
Published on Feb 9, 2019in bioRxiv
Janakiraman Udaiyappan (UA: University of Arizona), Jie Yu1
Estimated H-index: 1
(UA: University of Arizona)
+ 4 AuthorsMark A. Nelson32
Estimated H-index: 32
(UA: University of Arizona)
TAF1 intellectual disability syndrome is an X-linked disorder caused by loss-of-function mutations in the TAF1 gene. How these mutations cause dysmorphology, hypotonia, intellectual and motor defects is unknown. Mouse models which have embryonically targeted TAF1 have failed, possibly due to TAF1 being essential for viability, preferentially expressed in early brain development, and intolerant of mutation. Novel animal models are valuable tools for understanding neuronal pathology. Here, we repo...
Published on Sep 28, 2018
Sarah E. Hurst1
Estimated H-index: 1
(UA: University of Arizona),
Erika Liktor-Busa1
Estimated H-index: 1
(UA: University of Arizona)
+ 16 AuthorsKeri Ramsey16
Estimated H-index: 16
(TGen: Translational Genomics Research Institute)
We investigated the genome of a 5-year-old male who presented with global developmental delay (motor, cognitive, and speech), hypotonia, possibly ataxia, and cerebellar hypoplasia of unknown origin. Whole genome sequencing (WGS) and mRNA sequencing (RNA-seq) were performed on a family having an affected proband, his unaffected parents, and maternal grandfather. To explore the molecular and functional consequences of the variant, we performed cell proliferation assays, quantitative real-time PCR ...
Published on Aug 5, 2016
Margaret M. Briehl24
Estimated H-index: 24
,
Mark A. Nelson32
Estimated H-index: 32
+ 4 AuthorsRonald S. Weinstein48
Estimated H-index: 48
Faculty members from the Department of Pathology at The University of Arizona College of Medicine-Tucson have offered a 4-credit course on enhanced general pathology for graduate students since 1996. The course is titled, “Mechanisms of Human Disease.” Between 1997 and 2016, 270 graduate students completed Mechanisms of Human Disease. The students came from 21 programs of study. Analysis of Variance, using course grade as the dependent and degree, program, gender, and year (1997-2016) as indepen...
Published on Apr 1, 2016
Katherine E Hanlon4
Estimated H-index: 4
(UA: University of Arizona),
Alysia N. Lozano-Ondoua3
Estimated H-index: 3
(UA: University of Arizona)
+ 7 AuthorsTodd W. Vanderah56
Estimated H-index: 56
(UA: University of Arizona)
Introduction Cannabinoid compounds, both nonspecific as well as agonists selective for either cannabinoid receptor 1 (CB1) or cannabinoid receptor 2 (CB2), have been shown to modulate the tumor microenvironment by inducing apoptosis in tumor cells in several model systems. The mechanism of this modulation remains only partially delineated, and activity induced via the CB1 and CB2 receptors may be distinct despite significant sequence homology and structural similarity of ligands.
Published on Aug 19, 2015in FEBS Letters2.67
Melania E. Mercado-Pimentel8
Estimated H-index: 8
(UA: University of Arizona),
Benjamin C. Onyeagucha4
Estimated H-index: 4
(UA: University of Arizona)
+ 3 AuthorsMark A. Nelson32
Estimated H-index: 32
(UA: University of Arizona)
S100P signaling through the receptor for advanced glycation end-products (RAGE) contributes to colon cancer invasion and metastasis, but the mechanistic features of this process are obscure. Here, we investigate whether activation of S100P/RAGE signaling regulates oncogenic microRNA-21 (miR-21). We show that exogenous S100P up-regulates miR-21 levels in human colon cancer cells, whereas knockdown of S100P results in a decrease of miR-21. Furthermore, blockage of RAGE with anti-RAGE antibody supp...
Published on Jun 1, 2015in Supportive Care in Cancer2.75
Hani M. Babiker7
Estimated H-index: 7
(UA: University of Arizona),
Myke R. Green9
Estimated H-index: 9
(UA: University of Arizona)
+ 1 AuthorsEmad Elquza4
Estimated H-index: 4
(UA: University of Arizona)
Published on Jan 1, 2015
Octavian Bucur13
Estimated H-index: 13
,
Alexandru Almasan35
Estimated H-index: 35
+ 31 AuthorsKunej T1
Estimated H-index: 1
Published on Sep 1, 2013in Cancer Genetics and Cytogenetics2.18
Jennifer Hutchison2
Estimated H-index: 2
(UA: University of Arizona),
Zoe Cohen6
Estimated H-index: 6
(UA: University of Arizona)
+ 2 AuthorsMark A. Nelson32
Estimated H-index: 32
(UA: University of Arizona)
MicroRNAs have emerged as important post-translational regulators of gene expression and are involved in several physiological and pathological states including the pathogenesis of human colon cancers. In regards to tumor development, microRNAs can act as oncogenes or tumor suppressors. Two hereditary predispositions (i.e., Lynch syndrome and familial adenomatous polyposis) contribute to the development of colon cancer. In addition, individuals who suffer from inflammatory bowel diseases such as...
Published on Aug 1, 2013in Experimental Cell Research3.33
Benjamin C. Onyeagucha4
Estimated H-index: 4
(UA: University of Arizona),
Melania E. Mercado-Pimentel8
Estimated H-index: 8
(UA: University of Arizona)
+ 2 AuthorsMark A. Nelson32
Estimated H-index: 32
(UA: University of Arizona)
Accumulating evidence indicates that elevated S100P promotes the pathogenesis of cancers, including colon cancer. S100P exerts its effects by binding to and activating the Receptor for Advance Glycation End-products (RAGE). The effects of up-regulated S100P/RAGE signaling on cell functions are well documented. Despite these observations, little is known about the downstream targets of S100P/RAGE signaling. In the present study, we demonstrated for the first time that activation of RAGE by S100P ...
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