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Articles 1 - 30 of 35
Full-Text Articles in Other Genetics and Genomics
The Pros Of Changing Trna Identity, Michael Ibba
The Pros Of Changing Trna Identity, Michael Ibba
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
The notion that errors in protein synthesis are universally harmful to the cell has been questioned by findings that suggest such mistakes may sometimes be beneficial. However, how often these beneficial mistakes arise from programmed changes in gene expression as opposed to reduced accuracy of the translation machinery is still unclear. A new study published in JBC shows that some bacteria have beneficially evolved the ability to mistranslate specific parts of the genetic code, a trait that allows improved antibiotic resistance.
Induction Of Il19 Expression Through Jnk And Cgas-Sting Modulates Dna Damage–Induced Cytokine Production, Sara H. Small, E. Jessica Tang, Ryan L. Ragland, Yaroslava Ruzankina, David W. Schoppy, Rahul S. Mandal, M. Rebecca Glineburg, Zgjim Ustelenca, Daniel J. Powell, Fiona Simpkins, F. Bradley Johnson, Eric J. Brown
Induction Of Il19 Expression Through Jnk And Cgas-Sting Modulates Dna Damage–Induced Cytokine Production, Sara H. Small, E. Jessica Tang, Ryan L. Ragland, Yaroslava Ruzankina, David W. Schoppy, Rahul S. Mandal, M. Rebecca Glineburg, Zgjim Ustelenca, Daniel J. Powell, Fiona Simpkins, F. Bradley Johnson, Eric J. Brown
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
Cytokine production is a critical component of cell-extrinsic responses to DNA damage and cellular senescence. Here, we demonstrated that expression of the gene encoding interleukin-19 (IL-19) was enhanced by DNA damage through pathways mediated by c-Jun amino-terminal kinase (JNK) and cGAS-STING and that IL19 expression was required for the subsequent production of the cytokines IL-1, IL-6, and IL-8. IL19 expression was stimulated by diverse cellular stresses, including inhibition of the DNA replication checkpoint kinase ATR (ataxia telangiectasia and Rad3-related protein), oncogene expression, replicative exhaustion, oxidative stress, and DNA double-strand breaks. Unlike the production of IL-6 and IL-8, IL19 expression was …
The Effects Of Mapk Signaling On The Development Of Cerebellar Granule Cells, Kerry Morgan
The Effects Of Mapk Signaling On The Development Of Cerebellar Granule Cells, Kerry Morgan
University Scholar Projects
The granule cells are the most abundant neuronal type in the human brain. Rapid proliferation of granule cell progenitors results in dramatic expansion and folding of the cerebellar cortex during postnatal development. Mis-regulation of this proliferation process causes medulloblastoma, the most prevalent childhood brain tumor. In the developing cerebellum, granule cells are derived from Atoh1-expressing cells, which arise from the upper rhombic lip (the interface between the roof plate and neuroepithelium). In addition to granule cells, the Atoh1 lineage also gives rise to different types of neurons including cerebellar nuclei neurons. In the current study, I have investigated the …
The Effects Of Mapk Signaling On The Development Of Cerebellar Granule Cells, Kerry Morgan
The Effects Of Mapk Signaling On The Development Of Cerebellar Granule Cells, Kerry Morgan
Honors Scholar Theses
The granule cells are the most abundant neuronal type in the human brain. Rapid proliferation of granule cell progenitors results in dramatic expansion and folding of the cerebellar cortex during postnatal development. Mis-regulation of this proliferation process causes medulloblastoma, the most prevalent childhood brain tumor. In the developing cerebellum, granule cells are derived from Atoh1-expressing cells, which arise from the upper rhombic lip (the interface between the roof plate and neuroepithelium). In addition to granule cells, the Atoh1 lineage also gives rise to different types of neurons including cerebellar nuclei neurons. In the current study, I have investigated the …
Enhanced Detection Of Expanded Repeat Mrna Foci With Hybridization Chain Reaction, M. Rebecca Glineburg, Yuan Zhang, Amy Krans, Elizabeth M. Tank, Sami J. Barmada, Peter K. Todd
Enhanced Detection Of Expanded Repeat Mrna Foci With Hybridization Chain Reaction, M. Rebecca Glineburg, Yuan Zhang, Amy Krans, Elizabeth M. Tank, Sami J. Barmada, Peter K. Todd
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
Transcribed nucleotide repeat expansions form detectable RNA foci in patient cells that contribute to disease pathogenesis. The most widely used method for detecting RNA foci, fluorescence in situ hybridization (FISH), is powerful but can suffer from issues related to signal above background. Here we developed a repeat-specific form of hybridization chain reaction (R-HCR) as an alternative method for detection of repeat RNA foci in two neurodegenerative disorders: C9orf72 associated ALS and frontotemporal dementia (C9 ALS/FTD) and Fragile X-associated tremor/ataxia syndrome. R-HCR to both G4C2 and CGG repeats exhibited comparable specificity but > 40 × sensitivity compared to FISH, …
A "Choose-Your-Own" Classroom-Based Activity That Promotes Scientific Inquiry About Rna Interference, Jeremy L. Hsu
A "Choose-Your-Own" Classroom-Based Activity That Promotes Scientific Inquiry About Rna Interference, Jeremy L. Hsu
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
RNA interference (RNAi), the process that results in the degradation of a target gene’s mRNA, is a fundamental part of eukaryotic gene regulation and is also an important molecular technique that allows for experimental manipulation of gene expression without altering DNA sequences. Despite the importance of RNAi, there have been relatively few lecture-based activities designed to teach about the consequences of this process and counter common misconceptions. I present here an inquiry-based activity that is centered around a “choose your own experiment” design where students generate hypotheses and critically evaluate their ideas by choosing several simulated experiments. The activity presents …
Gmr36a08, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr36a08, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 49927
- ID - GMR36A08
- Location - 2R: 18120673, 18124576
- Base pairs - 3903
Gmr40e08, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr40e08, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 41238
- ID - GMR40E08
- Location - 2R: 18162090, 18165058
- Base pairs - 2968
Gmr42a07, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr42a07, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 45284
- ID - GMR42A07
- Location - 2R: 18146520, 18150306
- Base pairs - 3786
Gmr36a10, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr36a10, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 49373
- ID - GMR36A10
- Location - 2R: 18116788, 18120701
- Base pairs - 3913
Gmr40c09, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr40c09, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer
- ID - GMR40C09
- Location - 2R: 18132203, 18134987
- Base pairs - 2784
Gmr41f05, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr41f05, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 50133
- ID - GMR41F05
- Location - 2R: 18139042, 18142672
- Base pairs - 3630
Gmr35a04, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr35a04, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer
- ID - GMR35A04
- Location - 2R: 18125755, 18128365
- Base pairs - 2610
Gmr39h01, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr39h01, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 50066
- ID - GMR39H01
- Location - 2R: 18153797, 18156108
- Base pairs - 2311
Gmr42e10, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr42e10, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer
- ID - GMR42E10
- Location - 2R: 18133506, 18137474
- Base pairs - 3968
Gmr41c04, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr41c04, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer
- ID - GMR41C04
- Location -2R: 18143594, 18147064
- Base pairs - 3470
Gmr40c05, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr40c05, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 45682
- ID - GMR40C05
- Location - 2R: 18141630, 18144381
- Base pairs - 2751
Gmr41h07, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr41h07, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 46241
- ID - GMR41H07
- Location - 2R: 18150920, 18154671
- Base pairs - 3751
Gmr42h01, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
Gmr42h01, Anuradha Venkatakrishnan Chimata, Oorvashi Roy Puli, Amit Singh
DVE Enhancer Sequences Utilized in GMR Line
dve enhancer 48150
- ID - GMR42H01
- Location - 2R: 18158419, 18162751
- Base pairs - 4332
Deletion Of Uls1 Confers Damage Tolerance In Sgs1 Mutants Through A Top3-Dependent D-Loop Mediated Fork Restart Pathway, M. Rebecca Glineburg, Eleanor Johns, F. Brad Johnson
Deletion Of Uls1 Confers Damage Tolerance In Sgs1 Mutants Through A Top3-Dependent D-Loop Mediated Fork Restart Pathway, M. Rebecca Glineburg, Eleanor Johns, F. Brad Johnson
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
Homologous recombination (HR)-based repair during DNA replication can apparently utilize several partially overlapping repair pathways in response to any given lesion. A key player in HR repair is the Sgs1-Top3-Rmi1 (STR) complex, which is critical for resolving X-shaped recombination intermediates formed following bypass of methyl methanesulfonate (MMS)-induced damage. STR mutants are also sensitive to the ribonucleotide reductase inhibitor, hydroxyurea (HU), but unlike MMS treatment, HU treatment is not accompanied by X-structure accumulation, and it is thus unclear how STR functions in this context. Here we provide evidence that HU-induced fork stalling enlists Top3 prior to recombination intermediate formation. The resistance …
Unified Methods For Feature Selection In Large-Scale Genomic Studies With Censored Survival Outcomes, Lauren Spirko-Burns, Karthik Devarajan
Unified Methods For Feature Selection In Large-Scale Genomic Studies With Censored Survival Outcomes, Lauren Spirko-Burns, Karthik Devarajan
COBRA Preprint Series
One of the major goals in large-scale genomic studies is to identify genes with a prognostic impact on time-to-event outcomes which provide insight into the disease's process. With rapid developments in high-throughput genomic technologies in the past two decades, the scientific community is able to monitor the expression levels of tens of thousands of genes and proteins resulting in enormous data sets where the number of genomic features is far greater than the number of subjects. Methods based on univariate Cox regression are often used to select genomic features related to survival outcome; however, the Cox model assumes proportional hazards …
Supervised Dimension Reduction For Large-Scale "Omics" Data With Censored Survival Outcomes Under Possible Non-Proportional Hazards, Lauren Spirko-Burns, Karthik Devarajan
Supervised Dimension Reduction For Large-Scale "Omics" Data With Censored Survival Outcomes Under Possible Non-Proportional Hazards, Lauren Spirko-Burns, Karthik Devarajan
COBRA Preprint Series
The past two decades have witnessed significant advances in high-throughput ``omics" technologies such as genomics, proteomics, metabolomics, transcriptomics and radiomics. These technologies have enabled simultaneous measurement of the expression levels of tens of thousands of features from individual patient samples and have generated enormous amounts of data that require analysis and interpretation. One specific area of interest has been in studying the relationship between these features and patient outcomes, such as overall and recurrence-free survival, with the goal of developing a predictive ``omics" profile. Large-scale studies often suffer from the presence of a large fraction of censored observations and potential …
Hnrnpa2 Mediated Acetylation Reduces Telomere Length In Response To Mitochondrial Dysfunction, Manti Guha, Satish Srinivasan, F. Bradley Johnson, Gordon Ruthel, Kip Guja, Miguel Garcia-Diaz, Brett A. Kaufman, M. Rebecca Glineburg, Jikang Fang, Hiroshi Nakagawa, Jeelan Basha, Tapas Kundu, Narayan G. Avadhani
Hnrnpa2 Mediated Acetylation Reduces Telomere Length In Response To Mitochondrial Dysfunction, Manti Guha, Satish Srinivasan, F. Bradley Johnson, Gordon Ruthel, Kip Guja, Miguel Garcia-Diaz, Brett A. Kaufman, M. Rebecca Glineburg, Jikang Fang, Hiroshi Nakagawa, Jeelan Basha, Tapas Kundu, Narayan G. Avadhani
Biology, Chemistry, and Environmental Sciences Faculty Articles and Research
Telomeres protect against chromosomal damage. Accelerated telomere loss has been associated with premature aging syndromes such as Werner’s syndrome and Dyskeratosis Congenita, while, progressive telomere loss activates a DNA damage response leading to chromosomal instability, typically observed in cancer cells and senescent cells. Therefore, identifying mechanisms of telomere length maintenance is critical for understanding human pathologies. In this paper we demonstrate that mitochondrial dysfunction plays a causal role in telomere shortening. Furthermore, hnRNPA2, a mitochondrial stress responsive lysine acetyltransferase (KAT) acetylates telomere histone H4at lysine 8 of (H4K8) and this acetylation is associated with telomere attrition. Cells containing dysfunctional mitochondria …
45442 (Gmr18d08), Neha Gogia, Ankita Sarkar, Amit Singh
45442 (Gmr18d08), Neha Gogia, Ankita Sarkar, Amit Singh
Dpp Enhancer Sequences Utilized in GMR Line
dpp enhancer - 45442
- Id - GMR 18D08
- Location - 2L:2446783,2449086
- Base pairs – 2303 bp
45437 (Gmr18b08), Neha Gogia, Ankita Sarkar, Amit Singh
45437 (Gmr18b08), Neha Gogia, Ankita Sarkar, Amit Singh
Dpp Enhancer Sequences Utilized in GMR Line
dpp enhancer - 45437
- Id - GMR18B08
- Location - 2L:2455899,2457734
- Base pairs – 1835 bp
47472 (Gmr16g02), Neha Gogia, Ankita Sarkar, Amit Singh
47472 (Gmr16g02), Neha Gogia, Ankita Sarkar, Amit Singh
Dpp Enhancer Sequences Utilized in GMR Line
dpp enhancer - 47472
- Id - GMR16G02
- Location 2L:2425041, 2428154
- Base pairs – 3113 bp
48770 (Gmr17e04), Neha Gogia, Ankita Sarkar, Amit Singh
48770 (Gmr17e04), Neha Gogia, Ankita Sarkar, Amit Singh
Dpp Enhancer Sequences Utilized in GMR Line
dpp enhancer - 48770
- Id - GMR17E04
- Location 2L: 2428913..2432834
- Base pairs – 3921 bp
48784 (Gmr17g08), Neha Gogia, Ankita Sarkar, Amit Singh
48784 (Gmr17g08), Neha Gogia, Ankita Sarkar, Amit Singh
Dpp Enhancer Sequences Utilized in GMR Line
dpp enhancer - 48784
- Id - GMR 17G08
- Location 2L:2450278,2451074
- Base pairs – 796 bp
49283 (Gmr19c03), Neha Gogia, Ankita Sarkar, Amit Singh
49283 (Gmr19c03), Neha Gogia, Ankita Sarkar, Amit Singh
Dpp Enhancer Sequences Utilized in GMR Line
dpp enhancer - 49283
- Id - GMR19C03
- Location - 2L:2440970,2444735
- Base pairs – 3765 bp
48839 (Gmr19b04), Neha Gogia, Ankita Sarkar, Amit Singh
48839 (Gmr19b04), Neha Gogia, Ankita Sarkar, Amit Singh
Dpp Enhancer Sequences Utilized in GMR Line
dpp enhancer - 48839
- Id - GMR19B04,
- Location - 2L:2432214,2435785
- Base pairs – 3571 bp