MAYWOOD, Ill. - A new blood test can detect heart attacks hours faster than the current gold-standard blood test, according to a study led by Loyola University Chicago Stritch School of Medicine researchers.. The new test measures a protein that is released to the bloodstream by dying heart muscle. The protein is called cardiac myosin binding protein-C (cMyBP-C). The study found that cMyBP-C is released to the blood within just 15 minutes of cardiac damage, and rises to significant levels in three hours.. "This is a potential ultra-early biomarker that could confirm whether a patient has had a heart attack, leading to faster and more effective treatment," said Sakthivel Sadayappan, PhD, senior author of the study, published Dec. 13, 2013 in the American Journal of Physiology - Heart and Circulatory Physiology.. Between 60 and 70 percent of all patients who complain of chest pain do not have heart attacks. Many of these patients are admitted to the hospital, at considerable time and expense, ...
Figure 3. Identification of cardiac myosin binding protein-C (cMyBP-C) as a cardiac myocyte-specific PKGIα anti-remodeling substrate through molecular screen for PKGIa-LZ binding proteins. From Thoonen et al, 2015. (A) Outline of screening strategy. GST-fusion proteins were generated containing the PKGIa LZ domain (PKG1-59), the PKGIα mutated LZ domain (PKGLZM), or GST alone. The separate bait proteins were incubated with left ventricular protein lysates, followed by SDS PAGE and Coomassie staining. Protein bands selectively precipitating with PKG1-59 were removed and identified by mass spectroscopy. (B) Representative Coomassie stain from left ventricular protein lysates incubated with GST-fusion proteins. The 150 kDa band visible only in PKG1-59 precipitate (denoted by arrow) was excised and subjected to mass spectroscopy, revealing cMyBP-C as the predominant species. The thick bands between 25 and 30 kDa represent GST fusion proteins. Representative of 3 independent experiments. (C) Model ...
TY - JOUR. T1 - Cross-species mechanical fingerprinting of cardiac myosin binding protein-C. AU - Karsai, Árpád. AU - Kellermayer, Miklós S Z. AU - Harris, Samantha P.. PY - 2013/6/4. Y1 - 2013/6/4. N2 - Cardiac myosin binding protein-C (cMyBP-C) is a member of the immunoglobulin (Ig) superfamily of proteins and consists of 8 Ig- and 3 fibronectin III (FNIII)-like domains along with a unique regulatory sequence referred to as the MyBP-C motif or M-domain. We previously used atomic force microscopy to investigate the mechanical properties of murine cMyBP-C expressed using a baculovirus/insect cell expression system. Here, we investigate whether the mechanical properties of cMyBP-C are conserved across species by using atomic force microscopy to manipulate recombinant human cMyBP-C and native cMyBP-C purified from bovine heart. Force versus extension data obtained in velocity-clamp experiments showed that the mechanical response of the human recombinant protein was remarkably similar to that of ...
The histopathologic features of hypertrophic cardiomyopathy (HCM) are left ventricular hypertrophy, myocyte disarray, and interstitial fibrosis (1).. Cardiac magnetic resonance (CMR) is the gold standard for in vivo assessment of focal myocardial fibrosis using the late gadolinium enhancement (LGE) technique (2). This correlates with clinical risk factors for sudden death and arrhythmias, and is predictive of adverse outcomes including heart failure (3). It remains unclear how fibrosis evolves and how evolution correlates with ventricular remodeling. Our aim was to track long-term changes in CMR LGE in HCM over a 7-year follow-up period.. From 2001 to 2003, 59 patients with HCM (5 gene-positive for sarcomeric gene mutations with electrocardiogram changes fulfilling familial criteria) (1) underwent CMR LGE. Follow-up scans were performed in 12 patients on average 7.4 ± 0.4 years after the initial scans. The attrition of this overall high-risk cohort from a tertiary referral center occurred ...
van den Thillart, Guido, Dufour, Sylvie and Rankin, J. Cliff, eds. (2008) Spawning Migration of the European Eel. Fish & Fisheries Series, 30 . Springer Netherlands, London, UK. ISBN 978-1-4020-9095-0 (Online) Ababou, Abdessamad, Gautel, Mathias and Pfuhl, Mark (2007) Disecting the N-terminal myosin binding site of human cardiac myosin binding protein C : Structure and myosin binding of domain C2. Journal of Biological Chemistry, 282 (12). pp. 9204-9215. ISSN 00219258 Ahmed, Naveed, Tsang, Wing Y. and Page, Michael I. (2004) Acyl vs Sulfonyl Transfer in N-Acyl β-Sultams and 3-Oxo-β sultams. Organic Letters, 6 (2). pp. 201-203. ISSN 15237060 Akbar, Sirwan, Rout, Simon and Humphreys, Paul (2015) Draft Genome Sequences of Pseudomonas aeruginosa Strain PS3 and Citrobacter freundii Strain SA79 Obtained from a Wound DressingAssociated Biofilm. Genome Announcements, 3 (3). ISSN 2169-8287 Al-Nuaimi, Yusur, Hardman, Jonathan A., Bíró, Tamás, Haslam, Iain S., Philpott, Michael P., Tóth, Balázs I., ...
MYBPC1兔多克隆抗体(ab110363)可与人样本反应并经WB实验严格验证并得到3个独立的用户反馈。所有产品均提供质保服务,中国75%以上现货。
This case shows Ebstein anomaly with tricuspid regurgitation in an elderly patient. The anomaly was also demonstrated on echocardiography. Ebstein anomaly occurs in about 1 of every 200,000 live births and initial presentation by older patients ...
TY - JOUR. T1 - Preventative therapeutic approaches for hypertrophic cardiomyopathy. AU - Solomon, Tanya. AU - Filipovska, Aleksandra. AU - Hool, Livia. AU - Viola, Helena. PY - 2020/8/21. Y1 - 2020/8/21. N2 - Sarcomeric gene mutations are associated with the development of hypertrophic cardiomyopathy (HCM). Current drug therapeutics for HCM patients are effective in relieving symptoms, but do not prevent or reverse disease progression. Moreover, due to heterogeneity in the clinical manifestations of the disease, patients experience variable outcomes in response to therapeutics. Mechanistically, alterations in calcium handling, sarcomeric disorganization, energy metabolism and contractility participate in HCM disease progression. While some similarities exist, each mutation appears to lead to mutation-specific pathophysiology. Furthermore, these alterations may precede or proceed development of the pathology. This review assesses the efficacy of HCM therapeutics from studies performed in animal ...
Toxoplasma gondii is an obligate intracellular parasite that enters cells by a process of active penetration. Host cell penetration and parasite motility are driven by a myosin motor complex consisting of four known proteins: TgMyoA, an unconventional Class XIV myosin; TgMLC1, a myosin light chain; and two membrane-associated proteins, TgGAP45 and TgGAP50. Little is known about how the activity of the myosin motor complex is regulated. Here, we show that treatment of parasites with a recently identified small-molecule inhibitor of invasion and motility results in a rapid and irreversible change in the electrophoretic mobility of TgMLC1. While the precise nature of the TgMLC1 modification has not yet been established, it was mapped to the peptide Val46-Arg59. To determine if the TgMLC1 modification is responsible for the motility defect observed in parasites after compound treatment, the activity of myosin motor complexes from control and compound-treated parasites was compared in an in vitro ...
Hypertrophic cardiomyopathy (HCM), an inherited disease of the heart muscle, is among the most common Mendelian cardiac diseases, occurring in 1 in 500 people (1). Advances in genetics have facilitated identification of a subpopulation of patients with pathogenic variants in cardiac sarcomere genes. The earliest family mapped by positional cloning had a disease-causing mutation at position 403 of the β-myosin heavy chain (MHC) protein (2). A knock-in mouse model of this variant recapitulated aspects of human disease (3); many other sarcomere genes have been implicated subsequently (4). In clinics today, coding regions of numerous cardiac sarcomere genes are routinely sequenced, and, excluding those patients with discrete upper septal thickening, clearly pathogenic variants are identified in 30% to 50% of patients (5), thus marking a subset of "sarcomeric" HCM.. Current therapy for HCM is primarily palliative. Beta-blockers, nondihydropyridine calcium channel blockers, and the class Ia ...
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Mouse Primary Cells from Creative Bioarray are isolated from tissue of pathogen-free laboratory mice. Mouse Cells are grown in T25 tissue culture flasks pre-coated with gelatin-based solution for 0.5 hour and incubated in Creative Bioarrays Cell Culture Medium generally for 3-7 days. Cultures are then expanded. Prior to shipping, cells are detached from flasks and immediately cryo-preserved in vials. Each vial contains at least 1x10^6 cells per ml and is delivered frozen ...
Myosin Binding Protein-C (MyBP-C) comprises a family of accessory proteins that includes the cardiac, slow skeletal, and fast skeletal isoforms. The three isoforms share structural and sequence homology, and localize at the C-zone of the sarcomeric A-band where they interact with thick and thin filaments to regulate the cycling of actomyosin crossbridges. The cardiac isoform, encoded by MYBPC3, has been extensively studied over the last several decades due to its high mutational rate in congenital hypertrophic and dilated cardiomyopathy. It is only recently, however, that the MYBPC1 gene encoding the slow skeletal isoform (sMyBP-C) has gained attention. Accordingly, during the last five years it has been shown that MYBPC1 undergoes extensive exon shuffling resulting in the generation of multiple slow variants, which are co-expressed in different combinations and amounts in both slow and fast skeletal muscles. The sMyBP-C variants are subjected to PKA- and PKC-mediated phosphorylation in constitutive and
HCM - MedHelps HCM Center for Information, Symptoms, Resources, Treatments and Tools for HCM. Find HCM information, treatments for HCM and HCM symptoms.
Heritable cardiomyopathy (HCM) is the leading cause of sudden cardiac arrest (SCA) in young people, affecting 1 in 500 individuals. HCM is chiefly caused by mutations in myofibrillar proteins of the cardiac sarcomere, and cardiac myosin binding protein-C (cMyBP-C, encoded by MYBPC3) is one of the most commonly affected. cMyBP-C, an accessory protein that binds tightly to myosin, has an important role in thick filament regulation. Mice with genetic ablation of MYBPC3 exhibit cardiac hypertrophy, reduced ejection fraction, and increased relaxation times in vivo. Experiments with explanted hearts from these mice exhibit greater susceptibility to arrhythmias compared to WT, suggesting derangement of Ca2+ handling. The molecular mechanisms underlying the progression of HCM are poorly understood, and are difficult to tease apart in constitutive knock out models due to potential compensatory changes that can mask important aspects of the disease phenotype. We used a tamoxifen-induced conditional MYBPC3 ...
Rationale: A stable 40 kD fragment is produced from cardiac myosin binding protein-C (cMyBP-C) when the heart is stressed, using a stimulus such as ischemia reperfusion injury. Elevated levels of the fragment can be detected in both the diseased mouse and human heart but its ability to interfere with normal cardiac function in the intact animal is unexplored. Objective: To understand the potential pathogenicity of the 40 kD fragment in vivo and to investigate the molecular pathways that could be targeted for potential therapeutic intervention. Methods and Results: We generated cardiac myocyte-specific transgenic mice (TG) using a Tet-Off inducible system to permit controlled expression of the 40 kD fragment in cardiomyocytes. When 40 kD protein expression is induced by crossing the responder animals with tetracycline transactivator (tTA) mice under conditions where substantial quantities approximating those observed in disease hearts are reached, the double TG (DTG) mice subsequently develop ...
Ultrasonography is commonly used to diagnose left ventricular noncompaction (LVNC). A ratio of noncompacted to compacted myocardium (NC/C ratio) | |2 is often used to diagnose LVNC. However, a large proportion of patients with noncompact myocardium have NC/C | 2, and the prognosis of these patients have not been studied. We included children diagnosed with LVNC between 0 and 15 years of age from January 2007 to December 2018. LVNC was diagnosed based on Stöllberger standard when over three trabeculae were found to be associated with the interventricular recesses. A maximal end systolic ratio of noncompacted to compacted layers was NC/C ratio. Outcomes for LVNC subjects with NC/C | 2 and NC/C | 2 were compared using Kaplan-Meier methods. There were 124 newly diagnosed LVNC cases, classified as isolated (i-LVNC, n = 47) or non-isolated (ni-LVNC, n = 77) LVNC and NC/C | 2 (n = 43) or | 2 (n = 81). The median (interquartile range) follow-up duration was 12 (3-30) months for all patients and 16 (6-36)
Cardiac-specific myosin light chain kinase (cMLCK) is the kinase predominantly responsible for the maintenance of the basal level of phosphorylation of cardiac myosin light chain 2 (MLC2), which it phosphorylates at Ser-15. This phosphorylation repels the myosin heads from the thick myosin filament and moves them toward the thin actin filament. Unlike smooth muscle cells, MLC2 phosphorylation in striated muscle cells appears to be a positive modulator of Ca2+ sensitivity that shifts the Ca2+-force relationship toward the left and increases the maximal force response and thus does not initiate muscle contraction. Recent studies have revealed an increasing number of details of the biochemical, physiological, and pathophysiological characteristics of cMLCK. The combination of recent technological advances and the discovery of a novel class of biologically active nonstandard peptides will hopefully translate into the development of drugs for the treatment of heart diseases. (Circ J 2013; 77: ...
Left ventricular noncompaction (LVNC) is a cardiomyopathy associated with sporadic or familial disease, the latter having an autosomal dominant mode of transmission. The clinical features associated with LVNC vary from asymptomatic to symptomatic patients, with the potential for heart failure, supraventricular and ventricular arrhythmias, thromboembolic events, and sudden cardiac death. Echocardiography is the diagnostic modality of choice, revealing the pathognomonic features of a thick, bilayered myocardium; prominent ventricular trabeculations; and deep intertrabecular recesses. Widespread use and advances in the technology of echocardiography and cardiac magnetic resonance imaging are increasing awareness of LVNC, and cardiac magnetic resonance imaging is improving the ability to stage the severity of the disease and potential for adverse clinical consequences. Study of LVNC through research in embryology, imaging, and genetics has allowed enormous strides in the understanding of this heterogeneous
We describe a newborn infant with del(1)(q) syndrome, presenting with rare congenital cardiomyopathy and left ventricular noncompaction myocardium (LVNC), as well as typical clinical features such as facial dysmorphism and psychomotor retardation. Although conventional chromosome banding at 850 bands per haploid set indicated a karyotype of 46,XX,add(1)(q42.3), FISH analysis confirmed that the deleted portion was limited to within q43, and q44 was preserved. Therefore, the chromosome constitution is 46,XX,del(1)(q43q43), which has not previously been reported in the literature. Screening for the mutations in the candidate genes for LVNC, i.e. G4.5, CSX, Dystrobrevin, FKBP12, and Desmin, produced negative results. Interestingly, the deleted portion includes the locus for the cardiac ryanodine receptor type 2 gene (RyR2), that selectively binds to the FKBP12 homolog, FKBP12.6. The relationship between this rare myocardial abnormality and deletion of q43 is currently unknown and awaits further accumulation
Background There is controversy regarding the best echocardiographic diagnostic criteria for left ventricular noncompaction (LVNC). We assessed the diagnostic utility and reproducibility of the...
Introduction: The extreme variability in the phenotype and progression of hypertrophic cardiomyopathy (HCM) is still largely unexplained.. Hypothesis: Myocarditis can be a major cause of acute electrical instability or clinical deterioration in HCM patients.. Methods: One hundred-nineteen HCM patients (69M/50F, mean age 41±8 ys), 42 with acute clinical deterioration including electrical instability and/or rapidly worsening heart failure, and 77 clinically stable, underwent cardiac catheterization with left ventricular (LV) endomyocardial biopsy and gene analysis of major sarcomeric proteins. Biopsies were processed for histology, immunohistochemistry for inflammatory infiltrates characterization and polymerase chain reaction for the most common cardiotropic viruses. Controls were 50 normal surgical samples.. Results: All 119 patients showed histological findings suggestive of HCM. In addition CD45RO+ lymphocytes (≥14/mm2) with focal necrosis of the adjacent severely hypertrophied and often ...
The search for the heart fields dates to mapping studies carried out on embryos in the 1940s was the beginning of identifying lateral plate mesoderm that gives rise to cardiogenic cells and has the potential to for myocardium [7]. The heart field regions lie laterally to the primitive streak, with the subpharyngeal mesodermal progenitor cells of the secondary heart field (SHF) located medially and ventrally to the primary heart field (PHF) cells that give rise to the primary linear heart tube. The PHF and the SHF are adjacent within the heart field region of the lateral plate mesoderm and cardiac crescent (refer to student figure 2). It is understood that in the pharyngeal mesoderm the cardiac regions are "prepatterned" in the progenitor cell population [8], hence being termed "specified but undifferentiated". It is the patterning of cells within the soon to become myocardium, that is responsible differentiation into chamber-specific myocytes (atrial and ventricular) and conduction cells [9]. ...
Myomegalin has been characterized as a protein with the properties of a scaffold or structural protein that is expressed at high levels in skeletal and cardiac tissue, suggesting an important function in muscle, and which interacts with a cAMP-specific phosphodiesterase [13]. However, the precise function and interactions of this protein, and its five isoforms, have been largely unknown. We here describe how the smallest MMGL isoform, isoform 4, binds to known and predicted PKA targets in the cardiac myocyte, including some sarcomeric proteins, viz. cMyBPC, cTNI, ENO1, ENO3, CARP and COMMD4 (Tables 1 and 2). Moreover, we show that MMGL isoform 4 interacts with two regulatory subunits of PKA (Figure 3). Together these results describe MMGL isoform 4 as a novel sarcomeric AKAP, which, like mAKAP [14], is involved in assembling a PKA/PDE cAMP signalling module.. In addition to interacting with both types of regulatory subunits, viz. RI and RII, which qualifies MMGL isoform 4 as a dual-specific AKAP ...
The Syrian cardiomyopathic hamster (BIO14.6), that develops both muscular dystrophy and progressive cardiomyopathy, is widely used as an animal model of autosomal recessive cardiomyopathy mimicking human hypertrophic cardiomyopathy, and five genes have been proposed as strong candidates for the cause of cardiomyopathy. We recently mapped the cardiomyopathy locus of the hamster to the centromeric region of chromosome 9qa2.1-b1 by construction of a genetic linkage map of the Syrian hamster. Thus, we analyzed the loci of the five candidate genes, α tropomyosin, cardiac troponin T, adhalin, calpain 3 and cardiac myosin binding protein-C, by the FISH method, and found that these genes were mapped on the distal portion of chromosome 12qa5 and 4pa2 and the proximal portion of chromosomes 9qb7, 1qc1.1 and 1qb3, respectively. These results provide strong evidence that the five candidate genes previously proposed are not related to the hamster cardiomyopathy.. ...
臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。. To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of "NTU Repository" with "Academic Hub" to form NTU Scholars.. ...
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Ovariectomy fails to modify the cardiac myosin isoenzyme profile of adult rats.: Estrogen has been shown to help maintain the elevated expression of the high AT
About Heart Failure. Heart failure is a grievous condition that affects more than 23 million people worldwide, about half of whom have reduced left ventricular function. It is the leading cause of hospitalization and readmission in people age 65 and older. Despite broad use of standard treatments and advances in care, the prognosis for patients with heart failure is poor. An estimated one in five people over the age of 40 are at risk of developing heart failure, and approximately 50 percent of people diagnosed with heart failure will die within five years of initial hospitalization.. About Omecamtiv Mecarbil Omecamtiv mecarbil is a novel cardiac myosin activator. Cardiac myosin is the cytoskeletal motor protein in the cardiac muscle cell that is directly responsible for converting chemical energy into the mechanical force resulting in cardiac contraction. Cardiac myosin activators are thought to accelerate the rate-limiting step of the myosin enzymatic cycle and shift the enzymatic cycle in ...
Isolated ventricular non-compaction cardiomyopathy (IVNC) is a rare, morphologically distinct primary genetic cardiomyopathy, which is now gaining prominence as an important differential diagnosis in patients presenting with cardiac failure. We descr
New recommendations call for at-risk men aged 45-79 years to take aspirin daily to prevent a primary heart attack. Similarly, at-risk women aged 55-79 years should take aspirin to prevent a primary ischemic stroke.
TNNI3K兔多克隆抗体(ab86564)可与小鼠, 人样本反应并经WB实验严格验证,被1篇文献引用并得到1个独立的用户反馈。所有产品均提供质保服务,中国75%以上现货。
Cardiac myosin binding protein C phosphorylation affects cross-bridge cycles elementary steps in a site-specific manner.: Based on our recent finding that card
Mutations in the cardiac myosin binding protein C gene (MYBPC3) are common causes of hypertrophic cardiomyopathy (HCM) in humans. Even though the MYBPC3 E258K missense mutation is among the most prevalent HCM-causing mutations, the mechanism through which it causes disease remains unclear. We developed a novel neonatal murine 3D engineered cardiac tissue (ECT) model and previously presented data showing that Mybpc3 ablation (Mybpc3−/−) accelerates the kinetics of contraction and relaxation in the absence of hypertrophic remodeling in ECT. Furthermore, we showed that expression of wild type human MYBPC3 in Mybpc3−/− ECT (MYBPC3WT) restores contractile function. We hypothesized that adenoviral mediated expression of human E258K MYBPC3 in Mybpc3−/− ECT (MYBPC3E258K) would accelerate contractile kinetics and blunt the effect of dobutamine by abolishing phosphorylation-regulated inhibitory interactions between the C2-M-domain region of cMyBPC and myosin S2. The contractile characteristics ...
MYBPC3 encodes the cardiac isoform of myosin-binding protein C. Myosin-binding protein C is a myosin-associated protein found in the cross-bridge-bearing zone (C region) of A bands in striated muscle. MYBPC3, the cardiac isoform, is expressed exclussively in heart muscle. MYBPC gene is linked to CMH4 and demonstrated a splice donor mutationin 1 family with familial hypertrophic cardiomyopathy and a duplication mutation in a second. Both mutations were predicted to disrupt the high-affinity, C-terminal myosin-binding domain of cardiac MyBP-C. Again, findings demonstrated that as in the case of the 3 forms that had been defined in molecular terms previously, familial hypertrophic cardiomyopathy is a disease of the sarcomere.
Myosin light chain kinase (MLCK)-dependent phosphorylation of the regulatory light chain (RLC) of cardiac myosin is known to play a beneficial role in heart disease, but the idea of a phosphorylation-mediated reversal of a hypertrophic cardiomyopathy (HCM) phenotype is novel. Our previous studies on transgenic (Tg) HCM-RLC mice revealed that the D166V (Aspartate166 →Valine) mutation-induced changes in heart morphology and function coincided with largely reduced RLC phosphorylation in situ. In this paper, we hypothesized that the introduction of a constitutively phosphorylated Serine15 (S15D) into the hearts of D166V mice would prevent the development of a deleterious HCM phenotype. In support of this notion, MLCK-induced phosphorylation of D166V-mutated hearts was found to rescue some of their abnormal contractile properties. Tg-S15D-D166V mice were generated with the human cardiac RLC-S15D-D166V construct substituted for mouse cardiac RLC and were subjected to functional, structural, and ...
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Hypertrophic cardiomyopathy is a primary myocardial disorder with an autosomal pattern of inheritance, characterized by asymmetric left ventricular hypertrophy with myocyte and myofibrillar disarray. Approximately 30% to 50% of all cases are accounted for by mutations in the beta-cardiac myosin heavy chain gene on chromosome 14q1. Recent linkage analysis led to the association of the disease with additional loci on chromosomes 1q3, 11p13-q13, and 15q2, but the underlying gene defects are as yet unidentified. To date, about 34 mutations of the beta-cardiac myosin heavy chain gene have been described and shown to have important prognostic implications. Definite genotype-phenotype correlations have been described; however, wide diversity in cardiac morphology, pathophysiologic features, and clinical manifestations is still evident, even within the same family. The disease has an annual mortality of approximately 3%, related to both progressive heart failure and sudden cardiac death. Not o
A recent genome-wide association study identified the gene encoding lemur tyrosine kinase-2 (LMTK2) as a susceptibility gene for prostate cancer. The identified genetic alteration is within intron 9, but the mechanisms by which LMTK2 may impact upon prostate cancer are not clear because the functions of LMTK2 are poorly understood. Here, we show that LMTK2 regulates a known pathway that controls phosphorylation of kinesin-1 light chain-2 (KLC2) by glycogen synthase kinase-3β (GSK3β). KLC2 phosphorylation by GSK3β induces the release of cargo from KLC2. LMTK2 signals via protein phosphatase-1C (PP1C) to increase inhibitory phosphorylation of GSK3β on serine-9 that reduces KLC2 phosphorylation and promotes binding of the known KLC2 cargo Smad2. Smad2 signals to the nucleus in response to transforming growth factor-β (TGFβ) receptor stimulation and transport of Smad2 by kinesin-1 is required for this signalling. We show that small interfering RNA loss of LMTK2 not only reduces binding of ...
TY - JOUR. T1 - Contribution of the innate immune system to autoimmune myocarditis. T2 - A role for complement. AU - Kaya, Ziya. AU - Afanasyeva, Marina. AU - Wang, Yan. AU - Dohmen, K. Malte. AU - Schlichting, Jens. AU - Tretter, Theresa. AU - Fairweather, DeLisa. AU - Holers, V. Michael. AU - Rose, Noel R.. PY - 2001. Y1 - 2001. N2 - Myocarditis is a principal cause of heart disease among young adults and is often a precursor of heart failure due to dilated cardiomyopathy. We show here that complement is critical for the induction of experimental autoimmune myocarditis and that it acts through complement receptor type I (CR1) and type 2 (CR2). We also found a subset of CD44hiCD62Llo T cells that expresses CR1 and CR2 and propose that both receptors are involved in the expression of B and T cell activation markers, T cell proliferation and cytokine production. These findings provide a mechanism by which activated complement, a key product of the innate immune response, modulates the induction ...
BACKGROUND: Ebstein anomaly is a complex, congenital heart defect that is associated with a variety of cardiac abnormalities. Studies found a similar sarcomere gene mutation in patients with Ebstein anomaly (EA) and patients with isolated left ventricular non-compaction (LVNC). AIM: We aimed to show the prevalence of LVNC and its potential relationship with severe cardiac events (VT - ventricular tachycardia, cardiac arrest) in adult patients with EA. METHODS: We conducted a retrospective search of our institutional database from 2010 to 2014 for patients with EA and reviewed patients medical records (age, sex, clinical presentation, electrocardiographic, echocardiographic, and CMR - cardiac magnetic resonance features ...
TY - JOUR. T1 - Cannabidiol limits T cell-mediated chronic autoimmune myocarditis. T2 - Implications to autoimmune disorders and organ transplantation. AU - Lee, Wen Shin. AU - Erdelyi, Katalin. AU - Matyas, Csaba. AU - Mukhopadhyay, Partha. AU - Varga, Zoltan V.. AU - Liaudet, Lucas. AU - Haskó, G.. AU - Čiháková, Daniela. AU - Mechoulam, Raphael. AU - Pacher, Pal. PY - 2016. Y1 - 2016. N2 - Myocarditis is a major cause of heart failure and sudden cardiac death in young adults and adolescents. Many cases of myocarditis are associated with autoimmune processes in which cardiac myosin is a major autoantigen. Conventional immunosuppressive therapies often provide unsatisfactory results and are associated with adverse toxicities during the treatment of autoimmune myocarditis. Cannabidiol (CBD) is a nonpsychoactive constituent of marijuana that exerts antiinflammatory effects independent of classical cannabinoid receptors. Recently, 80 clinical trials have investigated the effects of CBD in ...
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The MYH7 gene is associated with autosomal dominant hypertrophic cardiomyopathy (HCM) (MedGen UID: 501195), dilated cardiomyopathy (DCM) (MedGen UID: 37831), left ventricular noncompaction (LVNC) (MedGen UID: 349005), and Laing distal myopathy (MPD1) (MedGen UID: 449370). It is also associated with autosomal dominant and recessive myosin storage myopathy (MSMA) (MedGen UID:374868). Additional MYH7-related conditions have also been reported (OMIM: 160760).
25 a ON OFF b MUTIPLE CROSS BRIDGES Q) u c S(/) "0 SINGLE CROSS BRIDGE time Fig. 6. A: Diagram of crossbridge cycle. Each crossbridge repeats attachment and detachment cycle. B: Sliding movement of bead driven by single and multiple crossbridges. In summary, we have utilized in vitro motility assay techniques to study the mechanical property of cardiac myosin under various conditions for different myosin isoforms. Although these findings were anticipated based on previous experiments with muscle preparations, this is the first presentation of such direct evidence at the molecular level. 13. J. Thyroxine induced redistribution of isozyme of rabbit ventricular myosin. Circ Res 50: 117 -124, 1982. 14. , et. al. Dynamic interaction between cardiac myosin isoforms modifies velocity of actomyosin sliding in vitro. Circ Res 73:696-704, 1993. 27 15. Barany, M. ATPase activity of myosin correlated with speed of muscle shortening. J Gen Physiol 50:197-218, 1967. 16. , Poggesi, C. et. al. Shortening ...
Traditionally, many diseases have been defined by their morphology and what better technique is there to demonstrate morphology in the living individual than imaging? Some diseases such as hypertrophic cardiomyopathy (HCM) started with a morphological sine qua non (2), with firm data about other aspects of their natural history coming much later. Many other morphological signatures of cardiac diseases are following a similar trajectory, especially with the widespread availability of sophisticated imaging. One such condition is left ventricular noncompaction (LV-NC)-a diagnosis primarily based on morphology-and unlike HCM, therein may lay a cautionary tale.. Imaging is a powerful technology, and with great power comes great responsibility and the need to use it wisely. The ability to see more and measure more does not necessarily increase ones ability to diagnose better or label pathology that has a good reason for needing a label. One has to only look at the coevolution of the availability of ...
Familial hypertrophic cardiomyopathy 12 information including symptoms, diagnosis, misdiagnosis, treatment, causes, patient stories, videos, forums, prevention, and prognosis.
European Society of Radiology: Could you please give a detailed overview of when and for which diseases you use cardiac imaging?. Yining Wang: Cardiac imaging is used for all the heart-related diseases when imaging evaluation is needed. For primary heart diseases such as coronary artery disease, congenital heart disease, primary cardiomyopathy, neoplastic disease and pericardial disease, we use cardiac imaging for screening, diagnosis and follow-up evaluation after treatment. For secondary diseases involving the heart, we use cardiac imaging for cardiac structural and functional assessment and follow-up evaluation after treatment.. ESR: Which modalities are usually used for what?. YW: Cardiac computed tomography (CT) is the most commonly used modality for coronary artery disease, however cardiac magnetic resonance (MR) is used to evaluate previous myocardial infarction and myocardial fibrosis. Cardiac CT and MR are used in combination for congenital heart disease and neoplastic disease.. Cardiac ...
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