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Heart RNA Decay

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https://www.readbyqxmd.com/read/26863136/in-silico-analysis-of-the-structural-and-biochemical-features-of-the-nmd-factor-upf1-in-ustilago-maydis
#1
Nancy Martínez-Montiel, Laura Morales-Lara, Julio M Hernández-Pérez, Rebeca D Martínez-Contreras
The molecular mechanisms regulating the accuracy of gene expression are still not fully understood. Among these mechanisms, Nonsense-mediated Decay (NMD) is a quality control process that detects post-transcriptionally abnormal transcripts and leads them to degradation. The UPF1 protein lays at the heart of NMD as shown by several structural and functional features reported for this factor mainly for Homo sapiens and Saccharomyces cerevisiae. This process is highly conserved in eukaryotes but functional diversity can be observed in various species...
2016: PloS One
https://www.readbyqxmd.com/read/26546742/microrna-7-a-mirna-with-expanding-roles-in-development-and-disease
#2
REVIEW
Jessica L Horsham, Clarissa Ganda, Felicity C Kalinowski, Rikki A M Brown, Michael R Epis, Peter J Leedman
MicroRNAs (miRNAs) are a family of short, non-coding RNA molecules (∼22nt) involved in post-transcriptional control of gene expression. They act via base-pairing with mRNA transcripts that harbour target sequences, resulting in accelerated mRNA decay and/or translational attenuation. Given miRNAs mediate the expression of molecules involved in many aspects of normal cell development and functioning, it is not surprising that aberrant miRNA expression is closely associated with many human diseases. Their pivotal role in driving a range of normal cellular physiology as well as pathological processes has established miRNAs as potential therapeutics, as well as potential diagnostic and prognostic tools in human health...
December 2015: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/26489465/post-transcriptional-regulation-of-nkx2-5-by-rhau-in-heart-development
#3
Junwei Nie, Mingyang Jiang, Xiaotian Zhang, Hao Tang, Hengwei Jin, Xinyi Huang, Baiyin Yuan, Chenxi Zhang, Janice Ching Lai, Yoshikuni Nagamine, Dejing Pan, Wengong Wang, Zhongzhou Yang
RNA G-quadruplexes (G4s) play important roles in RNA biology. However, the function and regulation of mRNA G-quadruplexes in embryonic development remain elusive. Previously, we identified RHAU (DHX36, G4R1) as an RNA helicase that resolves mRNA G-quadruplexes. Here, we find that cardiac deletion of Rhau leads to heart defects and embryonic lethality in mice. Gene expression profiling identified Nkx2-5 mRNA as a target of RHAU that associates with its 5' and 3' UTRs and modulates its stability and translation...
October 27, 2015: Cell Reports
https://www.readbyqxmd.com/read/25772296/contribution-of-sodium-channel-neuronal-isoform-nav1-1-to-late-sodium-current-in-ventricular-myocytes-from-failing-hearts
#4
Sudhish Mishra, Vitaliy Reznikov, Victor A Maltsev, Nidas A Undrovinas, Hani N Sabbah, Albertas Undrovinas
KEY POINTS: Late Na(+) current (INaL) contributes to action potential remodelling and Ca(2+)/Na(+) changes in heart failure. The molecular identity of INaL remains unclear. The contributions of different Na(+) channel isoforms, apart from the cardiac isoform, remain unknown. We discovered and characterized a substantial contribution of neuronal isoform Nav1.1 to INaL. This new component is physiologically relevant to the control of action potential shape and duration, as well as to cell Ca(2+) dynamics, especially in heart failure...
March 15, 2015: Journal of Physiology
https://www.readbyqxmd.com/read/25557785/improvement-of-smn2-pre-mrna-processing-mediated-by-exon-specific-u1-small-nuclear-rna
#5
Andrea Dal Mas, Malgorzata Ewa Rogalska, Erica Bussani, Franco Pagani
Exon-specific U1 snRNAs (ExSpe U1s) are modified U1 snRNAs that interact with intronic sequences downstream of the 5' splice site (ss) by complementarity. This process restores exon skipping caused by different types of mutation. We have investigated the molecular mechanism and activity of these molecules in spinal muscular atrophy (SMA), a genetic neuromuscular disease where a silent exonic transition on the survival motor neuron 2 (SMN2) leads to exon 7 (E7) skipping. By using different cellular models, we show that a single chromosome-integrated copy of ExSpe U1 induced a significant correction of endogenous SMN2 E7 splicing and resulted in the restoration of the corresponding SMN protein levels...
January 8, 2015: American Journal of Human Genetics
https://www.readbyqxmd.com/read/25516437/regulated-inositol-requiring-protein-1-dependent-decay-as-a-mechanism-of-corin-rna-and-protein-deficiency-in-advanced-human-systolic-heart-failure
#6
Rebecca Lee, Bin Xu, J Eduardo Rame, Leanne E Felkin, Paul Barton, Daniel L Dries
BACKGROUND: The compensatory actions of the endogenous natriuretic peptide system require adequate processing of natriuretic peptide pro‐hormones into biologically active, carboxyl‐terminal fragments. Natriuretic peptide pro‐peptide processing is accomplished by corin, a transmembrane serine protease expressed by cardiomyocytes. Brain natriuretic peptide (BNP) processing is inadequate in advanced heart failure and is independently associated with adverse outcomes; however, the molecular mechanisms causing impaired BNP processing are not understood...
December 2014: Journal of the American Heart Association
https://www.readbyqxmd.com/read/25326451/contribution-of-neuronal-isoform-nav1-1-to-late-sodium-current-in-ventricular-myocytes-from-failing-hearts
#7
Sudhish Mishra, Vitaliy Reznikov, Victor A Maltsev, Nidas A Undrovinas, Hani N Sabbah, Albertas Undrovinas
Late Na(+) current (INaL) contributes to action potential (AP) duration and Ca(2+) handling in cardiac cells. Augmented INaL was implicated in delayed repolarization and impaired Ca(2+) handling in heart failure (HF). We tested if Na(+) channel (Nav's) neuronal isoforms contribute to INaL and Ca(2+) cycling defects in HF in 17 dogs with HF achieved via sequential coronary artery embolizations. Six normal dogs served as control. Transient Na(+) current (INaT) and INaL in left ventricular cardiomyocytes (VCMs) were recorded by patch-clamp while Ca(2+) dynamics was monitored using fluo-4...
October 17, 2014: Journal of Physiology
https://www.readbyqxmd.com/read/25252951/progesterone-modulates-serca2a-expression-and-function-in-rabbit-cardiomyocytes
#8
Karni S Moshal, Zhe Zhang, Karim Roder, Tae Yun Kim, Leroy Cooper, Bogdan Patedakis Litvinov, Yichun Lu, Vishal Reddy, Dmitry Terentyev, Bum-Rak Choi, Gideon Koren
We recently showed that progesterone treatment abolished arrhythmias and sudden cardiac death in a transgenic rabbit model of long QT syndrome type 2 (LQT2). Moreover, levels of cardiac sarco(endo)plasmic reticulum Ca(2+)-ATPase type 2a (SERCA2a) were upregulated in LQT2 heart extracts. We hypothesized that progesterone treatment upregulated SERCA2a expression, thereby reducing Ca(2+)-dependent arrhythmias in LQT2 rabbits. We therefore investigated the effect of progesterone on SERCA2a regulation in isolated cardiomyocytes...
December 1, 2014: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/24361238/p38%C3%AE-regulates-serca2a-function
#9
Leena Kaikkonen, Johanna Magga, Veli-Pekka Ronkainen, Elina Koivisto, Ábel Perjes, J Kurt Chuprun, Leif Erik Vinge, Teemu Kilpiö, Jani Aro, Johanna Ulvila, Tarja Alakoski, James A Bibb, Istvan Szokodi, Walter J Koch, Heikki Ruskoaho, Risto Kerkelä
cAMP-dependent protein kinase (PKA) regulates the L-type calcium channel, the ryanodine receptor, and phospholamban (PLB) thereby increasing inotropy. Cardiac contractility is also regulated by p38 MAPK, which is a negative regulator of cardiac contractile function. The aim of this study was to identify the mechanism mediating the positive inotropic effect of p38 inhibition. Isolated adult and neonatal cardiomyocytes and perfused rat hearts were utilized to investigate the molecular mechanisms regulated by p38...
February 2014: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/24310933/a-case-of-pancreatic-agenesis-and-congenital-heart-defects-with-a-novel-gata6-nonsense-mutation-evidence-of-haploinsufficiency-due-to-nonsense-mediated-mrna-decay
#10
Shigeru Suzuki, Atsushi Nakao, Ashoor R Sarhat, Akiko Furuya, Kumihiro Matsuo, Yusuke Tanahashi, Hiroki Kajino, Hiroshi Azuma
Recently, GATA6 heterozygous loss-of-function mutations were reported to cause pancreatic agenesis and congenital heart defects (PACHD [OMIM:600001]). However, the molecular mechanisms resulting from premature termination codons have not been examined in this disorder. The objective of this study was to perform a genetic analysis of a patient with PACHD. A female patient presented with ventricular septal defect, patent ductus arteriosus, and congenital diaphragmatic hernia at birth. Permanent neonatal diabetes mellitus and pancreatic exocrine deficiency due to pancreatic agenesis was diagnosed at 1 month of age...
February 2014: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/24039113/clinical-and-neurocognitive-characterization-of-a-family-with-a-novel-med12-gene-frameshift-mutation
#11
Gaetan Lesca, Marie-Pierre Moizard, Gerald Bussy, Dominique Boggio, Hao Hu, Stefan A Haas, Hans-Hilger Ropers, Vera M Kalscheuer, Vincent Des Portes, Audrey Labalme, Damien Sanlaville, Patrick Edery, Martine Raynaud, James Lespinasse
FG syndrome, Lujan syndrome, and Ohdo syndrome, the Maat-Kievit-Brunner type, have been described as distinct syndromes with overlapping non-specific features and different missense mutations of the MED12 gene have been reported in all of them. We report a family including 10 males and 1 female affected with profound non-specific intellectual disability (ID) which was linked to a 30-cM region extending from Xp11.21 (ALAS2) to Xq22.3 (COL4A5). Parallel sequencing of all X-chromosome exons identified a frameshift mutation (c...
December 2013: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/23975932/dmd-transcript-imbalance-determines-dystrophin-levels
#12
Pietro Spitali, Janneke C van den Bergen, Ingrid E C Verhaart, Beatrijs Wokke, Anneke A M Janson, Rani van den Eijnde, Johan T den Dunnen, Jeroen F J Laros, Jan J G M Verschuuren, Peter A C 't Hoen, Annemieke Aartsma-Rus
Duchenne and Becker muscular dystrophies are caused by out-of-frame and in-frame mutations, respectively, in the dystrophin encoding DMD gene. Molecular therapies targeting the precursor-mRNA are in clinical trials and show promising results. These approaches will depend on the stability and expression levels of dystrophin mRNA in skeletal muscles and heart. We report that the DMD gene is more highly expressed in heart than in skeletal muscles, in mice and humans. The transcript mutated in the mdx mouse model shows a 5' to 3' imbalance compared with that of its wild-type counterpart and reading frame restoration via antisense-mediated exon skipping does not correct this event...
December 2013: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/23681777/staufen-mediated-mrna-decay
#13
REVIEW
Eonyoung Park, Lynne E Maquat
Staufen1 (STAU1)-mediated mRNA decay (SMD) is an mRNA degradation process in mammalian cells that is mediated by the binding of STAU1 to a STAU1-binding site (SBS) within the 3'-untranslated region (3'-UTR) of target mRNAs. During SMD, STAU1, a double-stranded (ds) RNA-binding protein, recognizes dsRNA structures formed either by intramolecular base pairing of 3'-UTR sequences or by intermolecular base pairing of 3'-UTR sequences with a long-noncoding RNA (lncRNA) via partially complementary Alu elements. Recently, STAU2, a paralog of STAU1, has also been reported to mediate SMD...
July 2013: Wiley Interdisciplinary Reviews. RNA
https://www.readbyqxmd.com/read/23448468/ulk1-plays-a-critical-role-in-ampk-mediated-myocardial-autophagy-and-contractile-dysfunction-following-acute-alcohol-challenge
#14
Machender R Kandadi, Nan Hu, Jun Ren
This study was designed to evaluate the role of ULK1 in AMPK-mediated myocardial autophagy and contractile dysfunction following acute alcohol challenge. Wild-type and AMPK knockout mice were challenged with ethanol (3 g/kg/d, i.p.) for 3 days. Myocardial function was evaluated using echocardiography and edge-detection. Western blot analysis was employed to evaluate the levels of AMPK, Raptor, mTOR, the AMPK downstream signal ULK1 and autophagy markers Beclin-1 and LC3-II. siRNA was used to knockdown ULK1 in H9C2 myoblasts...
2013: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/22280357/functional-null-mutations-in-the-gonosomal-homologue-gene-tbl1y-are-associated-with-non-syndromic-coarctation-of-the-aorta
#15
A Tagariello, C Breuer, Y Birkner, S Schmidt, A M Koch, R Cesnjevar, A Ruffer, S Dittrich, H Schneider, A Winterpacht, H Sticht, J Dotsch, O Toka
In patients with congenital heart defects, chromosomal anomalies are 100 times more frequent than in control subjects. Coarctation of the aorta can be detected in 15-20% of patients with Ullrich-Turner syndrome. By extensively reviewing literature involving breakpoint analysis of gonosomal deletions in Ullrich- Turner syndrome patients with and without coarctation of the aorta, we identified several gonosomal homolgous gene pairs of interest. Four of these homologous gene pairs were investigated by standard DNA sequencing in a cohort of 83 patients with non-syndromic coarctation of the aorta...
February 2012: Current Molecular Medicine
https://www.readbyqxmd.com/read/22180311/the-importance-of-celf-control-molecular-and-biological-roles-of-the-cug-bp-elav-like-family-of-rna-binding-proteins
#16
REVIEW
Twishasri Dasgupta, Andrea N Ladd
RNA processing is important for generating protein diversity and modulating levels of protein expression. The CUG-BP, Elav-like family (CELF) of RNA-binding proteins regulate several steps of RNA processing in the nucleus and cytoplasm, including pre-mRNA alternative splicing, C to U RNA editing, deadenylation, mRNA decay, and translation. In vivo, CELF proteins have been shown to play roles in gametogenesis and early embryonic development, heart and skeletal muscle function, and neurosynaptic transmission...
January 2012: Wiley Interdisciplinary Reviews. RNA
https://www.readbyqxmd.com/read/22079478/experimental-ssm-cvb3-infection-in-macaques
#17
Tiesuo Han, Wenqi He, Deguang Song, Kui Zhao, Chenchen Wu, Feng Gao, Huijun Lu, Xianying Gai, Xinrui Wang, Fei Li, Cuicui Ji, Xijuan Lin
OBJECTIVE: To evaluate the pathogenicity of SSM-CVB3 in a macaque model. METHODS: The clinical symptoms of macaques were recorded; hematological, biochemical and histopathological evaluations were completed; viral titers and neutralization titers (NT-titers) in sera were tested; and the mRNA levels of SSM-CVB3, coxsackievirus and adenovirus receptor (CAR) and decay accelerating factor (DAF) were determined. RESULTS: After SSM-CVB3 infection, the macaques showed a lack of activity, a poor appetite, a higher body temperature, and severe diarrhea...
February 2012: Experimental and Molecular Pathology
https://www.readbyqxmd.com/read/22057632/how-do-mybpc3-mutations-cause-hypertrophic-cardiomyopathy
#18
REVIEW
Steven Marston, O'Neal Copeland, Katja Gehmlich, Saskia Schlossarek, Lucie Carrier, Lucie Carrrier
It is well established that MYBPC3 mutations are the most common cause of hypertrophic cardiomyopathy, accounting for about half of identified mutations. However, when compared with mutations in other myofibrillar proteins that cause hypertrophic cardiomyopathy, MYBPC3 mutations seem to be the odd one out. The most striking characteristic of HCM mutations in MYBPC3 is that many are within introns and are predicted to cause aberrant splicing leading to a frameshift and a premature chain termination, yet the truncated peptides have never been identified in human heart tissue carrying these mutations...
May 2012: Journal of Muscle Research and Cell Motility
https://www.readbyqxmd.com/read/22009485/contractility-of-ventricular-myocytes-is-well-preserved-despite-altered-mechanisms-of-ca2-transport-and-a-changing-pattern-of-mrna-in-aged-type-2-zucker-diabetic-fatty-rat-heart
#19
F C Howarth, M A Qureshi, Z Hassan, D Isaev, K Parekh, A John, M Oz, H Raza, E Adeghate, T E Adrian
There has been a spectacular rise in the global prevalence of type 2 diabetes mellitus and cardiovascular complications are the major cause of morbidity and mortality in diabetic patients. The objective of the study was to investigate ventricular myocyte shortening, intracellular Ca(2+) signalling and expression of genes encoding cardiac muscle proteins in the aged Zucker diabetic fatty (ZDF) rat. There was a fourfold elevation in non-fasting blood glucose in ZDF rats (478.43 ± 29.22 mg/dl) compared to controls (108...
February 2012: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/21998310/functional-properties-of-a-newly-identified-c-terminal-splice-variant-of-cav1-3-l-type-ca2-channels
#20
Gabriella Bock, Mathias Gebhart, Anja Scharinger, Wanchana Jangsangthong, Perrine Busquet, Chiara Poggiani, Simone Sartori, Matteo E Mangoni, Martina J Sinnegger-Brauns, Stefan Herzig, Jörg Striessnig, Alexandra Koschak
An intramolecular interaction between a distal (DCRD) and a proximal regulatory domain (PCRD) within the C terminus of long Ca(v)1.3 L-type Ca(2+) channels (Ca(v)1.3(L)) is a major determinant of their voltage- and Ca(2+)-dependent gating kinetics. Removal of these regulatory domains by alternative splicing generates Ca(v)1.3(42A) channels that activate at a more negative voltage range and exhibit more pronounced Ca(2+)-dependent inactivation. Here we describe the discovery of a novel short splice variant (Ca(v)1...
December 9, 2011: Journal of Biological Chemistry
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