Sarcoplasmic Reticulum Calcium-Transporting ATPases
Ryanodine Receptor Calcium Release Channel
Excitation Contraction Coupling
Calcium Channels, L-Type
Muscle Fibers, Skeletal
Biological Transport, Active
Endoplasmic Reticulum Stress
Muscle Fibers, Fast-Twitch
Endoplasmic Reticulum, Rough
Amino Acid Sequence
Calcium Channel Blockers
Molecular Sequence Data
Inositol 1,4,5-Trisphosphate Receptors
Tacrolimus Binding Proteins
Endoplasmic Reticulum, Smooth
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Calcium Channel Agonists
Tacrolimus Binding Protein 1A
Ion Channel Gating
Dose-Response Relationship, Drug
Metals, Rare Earth
Muscle Fibers, Slow-Twitch
Electrophoresis, Polyacrylamide Gel
Muscle Relaxants, Central
Cyclic AMP-Dependent Protein Kinases
Cell Membrane Permeability
Receptors, Adrenergic, beta
Unfolded Protein Response
A novel interaction mechanism accounting for different acylphosphatase effects on cardiac and fast twitch skeletal muscle sarcoplasmic reticulum calcium pumps. (1/4498)In cardiac and skeletal muscle Ca2+ translocation from cytoplasm into sarcoplasmic reticulum (SR) is accomplished by different Ca2+-ATPases whose functioning involves the formation and decomposition of an acylphosphorylated phosphoenzyme intermediate (EP). In this study we found that acylphosphatase, an enzyme well represented in muscular tissues and which actively hydrolyzes EP, had different effects on heart (SERCA2a) and fast twitch skeletal muscle SR Ca2+-ATPase (SERCA1). With physiological acylphosphatase concentrations SERCA2a exhibited a parallel increase in the rates of both ATP hydrolysis and Ca2+ transport; in contrast, SERCA1 appeared to be uncoupled since the stimulation of ATP hydrolysis matched an inhibition of Ca2+ pump. These different effects probably depend on phospholamban, which is associated with SERCA2a but not SERCA1. Consistent with this view, the present study suggests that acylphosphatase-induced stimulation of SERCA2a, in addition to an enhanced EP hydrolysis, may be due to a displacement of phospholamban, thus to a removal of its inhibitory effect. (+info)
Expression of skeletal muscle sarcoplasmic reticulum calcium-ATPase is reduced in rats with postinfarction heart failure. (2/4498)OBJECTIVE: To determine whether heart failure in rats is associated with altered expression of the skeletal muscle sarcoplasmic reticulum Ca2+-ATPase (SERCA). METHODS: SERCA protein and mRNA were examined in the soleus muscles of eight female rats with heart failure induced by coronary artery ligation, six weeks after the procedure (mean (SEM) left ventricular end diastolic pressure 20.4 (2.2) mm Hg) and in six sham operated controls by western and northern analyses, respectively. RESULTS: SERCA-2a isoform protein was reduced by 16% (112 000 (4000) v 134 000 (2000) arbitrary units, p < 0.001), and SERCA-2a messenger RNA was reduced by 59% (0.24 (0. 06) v 0.58 (0.02) arbitrary units, p < 0.001). Although rats with heart failure had smaller muscles (0.54 mg/g v 0.66 mg/g body weight), no difference in locomotor activity was observed. CONCLUSIONS: These results may explain the previously documented abnormalities in calcium handling in skeletal muscle from animals with the same model of congestive heart failure, and could be responsible for the accelerated muscle fatigue characteristic of patients with heart failure. (+info)
Ca-releasing action of beta, gamma-methylene adenosine triphosphate on fragmented sarcoplasmic reticulum. (3/4498)beta,gamma-Methylene adenosine triphosphate (AMPOPCP) has two effects on fragmented sarcoplasmic reticulum (FSR), i.e., inhibition of the rate of Ca uptake and the induction of Ca release from FSR filled with Ca. The Ca release brought about by AMPOPCP has many features in common with the mechanism of Ca-induced Ca release: i) it is inhibited by 10 mM procaine; ii) the amount of Ca release increases with increase in the extent of saturation of FSR with Ca; iii) increase of the Ca concentration in the extent of saturation of FSR with Ca; iii) increase of the Ca concentration in the medium facilitates the release of Ca. However, no facilitation of Ca release upon decrease of Mg concentration in the medium is observable. AMPOPCP and caffeine potentiate each other remarkably in their Ca-releasing action, irrespective of the kind of substrate. From the mode of action of AMPOPCP on the rate of Ca uptake, the amount of phosphorylated intermediate (EP), and the effect on Sr release, it is suggested that the state of the FSR-ATP complex is crucial for Ca-induced Ca release. (+info)
Mutations of Arg198 in sarcoplasmic reticulum Ca2+-ATPase cause inhibition of hydrolysis of the phosphoenzyme intermediate formed from inorganic phosphate. (4/4498)Arg198 of sarcoplasmic reticulum Ca2+-ATPase was substituted with lysine, glutamine, glutamic acid, alanine, and isoleucine by site-directed mutagenesis. Kinetic analysis was performed with microsomal membranes isolated from COS-1 cells which were transfected with the mutated cDNAs. The rate of dephosphorylation of the ADP-insensitive phosphoenzyme was determined by first phosphorylating the Ca2+-ATPase with 32Pi and then diluting the sample with non-radioactive Pi. This rate was reduced substantially in the mutant R198Q, more strongly in the mutants R198A and R1981, and most strongly in the mutant R198E, but to a much lesser extent in R198K. The reduction in the rate of dephosphorylation was consistent with the observed decrease in the turnover rate of the Ca2+-ATPase accompanied by the steady-state accumulation of the ADP-insensitive phosphoenzyme formed from ATP. These results indicate that the positive charge and high hydrophilicity of Arg198 are critical for rapid hydrolysis of the ADP-insensitive phosphoenzyme. (+info)
A repetitive mode of activation of discrete Ca2+ release events (Ca2+ sparks) in frog skeletal muscle fibres. (5/4498)1. Ca2+ release events (Ca2+ 'sparks'), which are believed to arise from the opening of a sarcoplasmic reticulum (SR) Ca2+ release channel or a small cluster of such channels that act as a release unit, have been measured in single, frog (Rana pipiens) skeletal muscle fibres. 2. Under conditions of extremely low rates of occurrence of Ca2+ sparks we observed, within individual identified triads, repetitive Ca2+ release events which occurred at a frequency more than 100-fold greater than the prevailing average event rate. Repetitive sparks were recorded during voltage-clamp test depolarizations after a brief (0.3-2 s) repriming interval in fibres held at 0 mV and in chronically depolarized, 'notched' fibres. 3. These repetitive events are likely to arise from the re-opening of the same SR Ca2+ release channel or release unit operating in a repetitive gating mode ('rep-mode'), rather than from the random activation of multiple, independent channels or release units within a triad. A train of rep-mode events thus represents a series of Ca2+ sparks arising from a single location within the fibre. Rep-mode events are activated among different triads in a random manner after brief repriming. The frequency of repetitive events among all identified events during voltage-clamp depolarization to 0 mV after brief repriming was 3.9 +/- 1.3 %. The occurrence of repetitive events was not related to exposure of the fibre to laser illumination. 4. The events observed within a rep-mode train exhibited a relatively uniform amplitude. Analysis of intervals between identified events in triads exhibiting rep-mode trains indicated similar variations of fluorescence as in neighbouring, quiescent triads, suggesting there was not a significant number of small, unidentified events at the triads exhibiting rep-mode activity. 5. The distribution of rep-mode interspark intervals exhibited a paucity of events at short intervals, consistent with the need for recovery from inactivation before activation of the next event in a repetitive train. The mean interspark interval of repetitive sparks during voltage-clamp depolarizations was 88 +/- 5 ms, and was independent of membrane potential. 6. The individual Ca2+ sparks within a rep-mode train were similar in average amplitude and spatiotemporal extent to singly occurring sparks, suggesting a common mechanism for termination of the channel opening(s) underlying both types of events. The average properties of the sparks did not vary during a train. The relative amplitude of a spark within a rep-mode was not correlated with its rise time. 7. Repetitive Ca2+ release events represent a mode of gating of SR Ca2+ release channels which may be significant during long depolarizations and which may be influenced by the biochemical state of the SR ryanodine receptor Ca2+ release channels. (+info)
Local control models of cardiac excitation-contraction coupling. A possible role for allosteric interactions between ryanodine receptors. (6/4498)In cardiac muscle, release of activator calcium from the sarcoplasmic reticulum occurs by calcium- induced calcium release through ryanodine receptors (RyRs), which are clustered in a dense, regular, two-dimensional lattice array at the diad junction. We simulated numerically the stochastic dynamics of RyRs and L-type sarcolemmal calcium channels interacting via calcium nano-domains in the junctional cleft. Four putative RyR gating schemes based on single-channel measurements in lipid bilayers all failed to give stable excitation-contraction coupling, due either to insufficiently strong inactivation to terminate locally regenerative calcium-induced calcium release or insufficient cooperativity to discriminate against RyR activation by background calcium. If the ryanodine receptor was represented, instead, by a phenomenological four-state gating scheme, with channel opening resulting from simultaneous binding of two Ca2+ ions, and either calcium-dependent or activation-linked inactivation, the simulations gave a good semiquantitative accounting for the macroscopic features of excitation-contraction coupling. It was possible to restore stability to a model based on a bilayer-derived gating scheme, by introducing allosteric interactions between nearest-neighbor RyRs so as to stabilize the inactivated state and produce cooperativity among calcium binding sites on different RyRs. Such allosteric coupling between RyRs may be a function of the foot process and lattice array, explaining their conservation during evolution. (+info)
Cellular mechanisms of altered contractility in the hypertrophied heart: big hearts, big sparks. (7/4498)To investigate the cellular mechanisms for altered Ca2+ homeostasis and contractility in cardiac hypertrophy, we measured whole-cell L-type Ca2+ currents (ICa,L), whole-cell Ca2+ transients ([Ca2+]i), and Ca2+ sparks in ventricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age- and sex-matched Wistar-Kyoto and Sprague-Dawley control rats. By echocardiography, SHR hearts had cardiac hypertrophy and enhanced contractility (increased fractional shortening) and no signs of heart failure. SHR cells had a voltage-dependent increase in peak [Ca2+]i amplitude (at 0 mV, 1330+/-62 nmol/L [SHRs] versus 836+/-48 nmol/L [controls], P<0.05) that was not associated with changes in ICa,L density or kinetics, resting [Ca2+]i, or Ca2+ content of the sarcoplasmic reticulum (SR). SHR cells had increased time of relaxation. Ca2+ sparks from SHR cells had larger average amplitudes (173+/-192 nmol/L [SHRs] versus 109+/-64 nmol/L [control]; P<0.05), which was due to redistribution of Ca2+ sparks to a larger amplitude population. This change in Ca2+ spark amplitude distribution was not associated with any change in the density of ryanodine receptors, calsequestrin, junctin, triadin 1, Ca2+-ATPase, or phospholamban. Therefore, SHRs with cardiac hypertrophy have increased contractility, [Ca2+]i amplitude, time to relaxation, and average Ca2+ spark amplitude ("big sparks"). Importantly, big sparks occurred without alteration in the trigger for SR Ca2+ release (ICa,L), SR Ca2+ content, or the expression of several SR Ca2+-cycling proteins. Thus, cardiac hypertrophy in SHRs is linked with an alteration in the coupling of Ca2+ entry through L-type Ca2+ channels and the release of Ca2+ from the SR, leading to big sparks and enhanced contractility. Alterations in the microdomain between L-type Ca2+ channels and SR Ca2+ release channels may underlie the changes in Ca2+ homeostasis observed in cardiac hypertrophy. Modulation of SR Ca2+ release may provide a new therapeutic strategy for cardiac hypertrophy and for its progression to heart failure and sudden death. (+info)
The sarcoplasmic reticulum and the Na+/Ca2+ exchanger both contribute to the Ca2+ transient of failing human ventricular myocytes. (8/4498)Our objective was to determine the respective roles of the sarcoplasmic reticulum (SR) and the Na+/Ca2+ exchanger in the small, slowly decaying Ca2+ transients of failing human ventricular myocytes. Left ventricular myocytes were isolated from explanted hearts of patients with severe heart failure (n=18). Cytosolic Ca2+, contraction, and action potentials were measured by using indo-1, edge detection, and patch pipettes, respectively. Selective inhibitors of SR Ca2+ transport (thapsigargin) and reverse-mode Na+/Ca2+ exchange activity (No. 7943, Kanebo Ltd) were used to define the respective contribution of these processes to the Ca2+ transient. Ca2+ transients and contractions induced by action potentials (AP transients) at 0.5 Hz exhibited phasic and tonic components. The duration of the tonic component was determined by the action potential duration. Ca2+ transients induced by caffeine (Caf transients) exhibited only a phasic component with a rapid rate of decay that was dependent on extracellular Na+. The SR Ca2+-ATPase inhibitor thapsigargin abolished the phasic component of the AP Ca2+ transient and of the Caf transient but had no significant effect on the tonic component of the AP transient. The Na+/Ca2+ exchange inhibitor No. 7943 eliminated the tonic component of the AP transient and reduced the magnitude of the phasic component. In failing human myocytes, Ca2+ transients and contractions exhibit an SR-related, phasic component and a slow, reverse-mode Na+/Ca2+ exchange-related tonic component. These findings suggest that Ca2+ influx via reverse-mode Na+/Ca2+ exchange during the action potential may contribute to the slow decay of the Ca2+ transient in failing human myocytes. (+info)
The exact cause of malignant hyperthermia is not fully understood, but it is believed to be related to a genetic predisposition and exposure to certain anesthetic agents. The condition can be triggered by a variety of factors, including the use of certain anesthetics, stimulation of the sympathetic nervous system, and changes in blood sugar levels.
Symptoms of malignant hyperthermia can include:
* Elevated body temperature (usually above 104°F/40°C)
* Muscle rigidity and stiffness
* Heart arrhythmias and palpitations
* Shivering or tremors
* Confusion, agitation, or other neurological symptoms
* Shortness of breath or respiratory failure
If left untreated, malignant hyperthermia can lead to serious complications such as seizures, brain damage, and even death. Treatment typically involves the immediate discontinuation of any triggering anesthetic agents, cooling measures such as ice packs or cold compresses, and medications to help regulate body temperature and reduce muscle rigidity. In severe cases, mechanical ventilation may be necessary to support breathing.
Overall, malignant hyperthermia is a rare but potentially life-threatening condition that requires prompt recognition and treatment to prevent serious complications and improve outcomes.
Medical Term: Cardiomegaly
Definition: An abnormal enlargement of the heart.
Symptoms: Difficulty breathing, shortness of breath, fatigue, swelling of legs and feet, chest pain, and palpitations.
Causes: Hypertension, cardiac valve disease, myocardial infarction (heart attack), congenital heart defects, and other conditions that affect the heart muscle or cardiovascular system.
Diagnosis: Physical examination, electrocardiogram (ECG), chest x-ray, echocardiography, and other diagnostic tests as necessary.
Treatment: Medications such as diuretics, vasodilators, and beta blockers, lifestyle changes such as exercise and diet modifications, surgery or other interventions in severe cases.
Note: Cardiomegaly is a serious medical condition that requires prompt diagnosis and treatment to prevent complications such as heart failure and death. If you suspect you or someone else may have cardiomegaly, seek medical attention immediately.
There are many different types of cardiac arrhythmias, including:
1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.
Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.
There are two main types of heart failure:
1. Left-sided heart failure: This occurs when the left ventricle, which is the main pumping chamber of the heart, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the lungs and other organs.
2. Right-sided heart failure: This occurs when the right ventricle, which pumps blood to the lungs, becomes weakened and is unable to pump blood effectively. This can lead to congestion in the body's tissues and organs.
Symptoms of heart failure may include:
* Shortness of breath
* Swelling in the legs, ankles, and feet
* Swelling in the abdomen
* Weight gain
* Coughing up pink, frothy fluid
* Rapid or irregular heartbeat
* Dizziness or lightheadedness
Treatment for heart failure typically involves a combination of medications and lifestyle changes. Medications may include diuretics to remove excess fluid from the body, ACE inhibitors or beta blockers to reduce blood pressure and improve blood flow, and aldosterone antagonists to reduce the amount of fluid in the body. Lifestyle changes may include a healthy diet, regular exercise, and stress reduction techniques. In severe cases, heart failure may require hospitalization or implantation of a device such as an implantable cardioverter-defibrillator (ICD) or a left ventricular assist device (LVAD).
It is important to note that heart failure is a chronic condition, and it requires ongoing management and monitoring to prevent complications and improve quality of life. With proper treatment and lifestyle changes, many people with heart failure are able to manage their symptoms and lead active lives.
There are several types of cardiomyopathies, each with distinct characteristics and symptoms. Some of the most common forms of cardiomyopathy include:
1. Hypertrophic cardiomyopathy (HCM): This is the most common form of cardiomyopathy and is characterized by an abnormal thickening of the heart muscle, particularly in the left ventricle. HCM can lead to obstruction of the left ventricular outflow tract and can increase the risk of sudden death.
2. Dilated cardiomyopathy: This type of cardiomyopathy is characterized by a decrease in the heart's ability to pump blood effectively, leading to enlargement of the heart and potentially life-threatening complications such as congestive heart failure.
3. Restrictive cardiomyopathy: This type of cardiomyopathy is characterized by stiffness of the heart muscle, which makes it difficult for the heart to fill with blood. This can lead to shortness of breath and fatigue.
4. Left ventricular non-compaction (LVNC): This is a rare type of cardiomyopathy that occurs when the left ventricle does not properly compact, leading to reduced cardiac function and potentially life-threatening complications.
5. Cardiac amyloidosis: This is a condition in which abnormal proteins accumulate in the heart tissue, leading to stiffness and impaired cardiac function.
6. Right ventricular cardiomyopathy (RVCM): This type of cardiomyopathy is characterized by impaired function of the right ventricle, which can lead to complications such as pulmonary hypertension and heart failure.
7. Endocardial fibroelastoma: This is a rare type of cardiomyopathy that occurs when abnormal tissue grows on the inner lining of the heart, leading to reduced cardiac function and potentially life-threatening complications.
8. Cardiac sarcoidosis: This is a condition in which inflammatory cells accumulate in the heart, leading to impaired cardiac function and potentially life-threatening complications.
9. Hypertrophic cardiomyopathy (HCM): This is a condition in which the heart muscle thickens, leading to reduced cardiac function and potentially life-threatening complications such as arrhythmias and sudden death.
10. Hypokinetic left ventricular cardiomyopathy: This type of cardiomyopathy is characterized by decreased contraction of the left ventricle, leading to reduced cardiac function and potentially life-threatening complications such as heart failure.
It's important to note that some of these types of cardiomyopathy are more common in certain populations, such as hypertrophic cardiomyopathy being more common in young athletes. Additionally, some types of cardiomyopathy may have overlapping symptoms or co-occurring conditions, so it's important to work with a healthcare provider for an accurate diagnosis and appropriate treatment.
Cardiac output is typically measured using invasive or non-invasive methods. Invasive methods involve inserting a catheter into the heart to directly measure cardiac output. Non-invasive methods include echocardiography, MRI, and CT scans. These tests can provide an estimate of cardiac output based on the volume of blood being pumped out of the heart and the rate at which it is being pumped.
There are several factors that can contribute to low cardiac output. These include:
1. Heart failure: This occurs when the heart is unable to pump enough blood to meet the body's needs, leading to fatigue and shortness of breath.
2. Anemia: A low red blood cell count can reduce the amount of oxygen being delivered to the body's tissues, leading to fatigue and weakness.
3. Medication side effects: Certain medications, such as beta blockers, can slow down the heart rate and reduce cardiac output.
4. Sepsis: A severe infection can lead to inflammation throughout the body, which can affect the heart's ability to pump blood effectively.
5. Myocardial infarction (heart attack): This occurs when the heart muscle is damaged due to a lack of oxygen, leading to reduced cardiac output.
Low cardiac output can cause a range of symptoms, including:
1. Fatigue and weakness
2. Dizziness and lightheadedness
3. Shortness of breath
4. Pale skin
5. Decreased urine output
6. Confusion and disorientation
The treatment of low cardiac output depends on the underlying cause. Treatment may include:
1. Medications to increase heart rate and contractility
2. Diuretics to reduce fluid buildup in the body
3. Oxygen therapy to increase oxygenation of tissues
4. Mechanical support devices, such as intra-aortic balloon pumps or ventricular assist devices
5. Surgery to repair or replace damaged heart tissue
6. Lifestyle changes, such as a healthy diet and regular exercise, to improve cardiovascular health.
Preventing low cardiac output involves managing any underlying medical conditions, taking medications as directed, and making lifestyle changes to improve cardiovascular health. This may include:
1. Monitoring and controlling blood pressure
2. Managing diabetes and other chronic conditions
3. Avoiding substances that can damage the heart, such as tobacco and excessive alcohol
4. Exercising regularly
5. Eating a healthy diet that is low in saturated fats and cholesterol
6. Maintaining a healthy weight.
1. Muscular dystrophy: A group of genetic disorders characterized by progressive muscle weakness and degeneration.
2. Myopathy: A condition where the muscles become damaged or diseased, leading to muscle weakness and wasting.
3. Fibromyalgia: A chronic condition characterized by widespread pain, fatigue, and muscle stiffness.
4. Rhabdomyolysis: A condition where the muscle tissue is damaged, leading to the release of myoglobin into the bloodstream and potentially causing kidney damage.
5. Polymyositis/dermatomyositis: Inflammatory conditions that affect the muscles and skin.
6. Muscle strain: A common injury caused by overstretching or tearing of muscle fibers.
7. Cervical dystonia: A movement disorder characterized by involuntary contractions of the neck muscles.
8. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, leading to muscle weakness and fatigue.
9. Oculopharyngeal myopathy: A condition characterized by weakness of the muscles used for swallowing and eye movements.
10. Inclusion body myositis: An inflammatory condition that affects the muscles, leading to progressive muscle weakness and wasting.
These are just a few examples of the many different types of muscular diseases that can affect individuals. Each condition has its unique set of symptoms, causes, and treatment options. It's important for individuals experiencing muscle weakness or wasting to seek medical attention to receive an accurate diagnosis and appropriate care.
Source: Genetic and Rare Diseases Information Center (GARD), the National Institutes of Health (NIH)
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
David W. Deamer
Calcium-induced calcium release
Striated muscle tissue
Catecholaminergic polymorphic ventricular tachycardia
Arnold Martin Katz
Cardiac action potential
Physiological effects in space
Discovery and development of beta-blockers
Keith R. Porter
Index of biochemistry articles
Unfolded protein response
List of MeSH codes (A11)
Identification of a 97-kDa Mastoparan-Binding Protein Involving in Ca2+ Release from Skeletal Muscle Sarcoplasmic Reticulum |...
Disuse-associated loss of the protease LONP1 in muscle impairs mitochondrial function and causes reduced skeletal muscle mass...
Daniel Bradley : Trinity Research - Trinity College Dublin
IgE-dependent human basophil responses are inversely associated with the sarcoplasmic reticulum Ca 2+ -ATPase (SERCA) - Kent...
A kink in DWORF helical structure controls the activation of the sarcoplasmic reticulum Ca|sup|2+|/sup|-ATPase. | Structure;30...
IJMS | Free Full-Text | Brain RNA-Seq Profiling of the Mucopolysaccharidosis Type II Mouse Model
Calmodulin modulates initiation but not termination of spontaneous Ca2+ sparks in frog skeletal muscle
Darier disease: MedlinePlus Genetics
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Middle Cerebral Artery Stroke: Overview, Rehabilitation Setting Selection and Indications, Best Practices
SERCA1 ATPase Antibody (4B8) (H00000487-M05): Novus Biologicals
MESH TREE NUMBER CHANGES - 2008 MeSH
Staff Listing - The University of Nottingham
William Clusin, MD | Stanford Medicine
Nervous System Health And Social Care - 990 Words | AntiEssays
Pressure Injuries (Pressure Ulcers) and Wound Care Medication: Skeletal Muscle Relaxants (Centrally Acting), Skeletal Muscle...
Flashcards - Histo Lecutre 15
JCI Insight - Volume 4, Issue 17
JCI - Volume 93, Issue 3
Calcium and Disease: Hypertension, organ calcification, & shock, vs. respiratory energy
Dynamic and Configurational Approach to the Glass Transition by Nanoscale Cooperativity
Energy and Epigenetics 3: Autoimmunity, Cancer, Autism - Dr. Jack Kruse
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MH-Susceptibility and Operating Room Personnel: Defining the Risks - MHAUS
- This enzyme acts as a pump that helps control the level of positively charged calcium atoms (calcium ions) inside cells, particularly in the endoplasmic reticulum and the sarcoplasmic reticulum. (medlineplus.gov)
- A lack of SERCA2 enzyme reduces calcium levels in the endoplasmic reticulum, causing it to become dysfunctional. (medlineplus.gov)
- Calmodulin is a ubiquitous Ca(2+) sensing protein that binds to and modulates the sarcoplasmic reticulum Ca(2+) release channel, ryanodine receptor (RYR). (nih.gov)
- An N-terminal extension of calmodulin, (N+3)calmodulin, that binds to but does not activate RYR at nM [Ca(2+)] in sarcoplasmic reticulum vesicles, prevented the calmodulin-induced increase in spark frequency. (nih.gov)
- On models of biological membranes, sarcoplasmic reticulum vesicles and isolated myocardial muscles, it has been shown that reactive oxygen species and redox systems of the cell participate in the regulation of calcium transfer through the ion channels of the membranes. (cardioweb.ru)
- In the sarcoplasmic reticulum membrane, PLN binds to the sarco(endo)plasmic reticulum Ca 2+ -ATPase (SERCA), keeping this enzyme's function within a narrow physiological window. (elifesciences.org)
- Direct-acting skeletal muscle relaxants inhibit muscle contraction by decreasing calcium release from the sarcoplasmic reticulum in muscle cells. (medscape.com)
- Sequencing of genes involved in the movement of calcium across human skeletal muscle sarcoplasmic reticulum: continuing the search for genes associated with malignant hyperthermia. (cdc.gov)
- Previous studies suggest that the sarcoplasmic reticulum Ca2+-ATPase (SERCA2), which regulates cytosolic calcium levels, may be inversely associated with airway smooth muscle reactivity in asthma. (kent.ac.uk)
- This enzyme catalyzes the hydrolysis of ATP coupled with the translocation of calcium from the cytosol to the sarcoplasmic reticulum lumen, and is involved in muscular excitation and contraction. (novusbio.com)
- Organization of junctional sarcoplasmic reticulum proteins in skeletal muscle fibers. (nih.gov)
- acts on Ca(2+)-induced Ca(2+) release channels of skeletal muscle sarcoplasmic reticulum. (nih.gov)
- 6. Properties of Ca(2+) release induced by clofibric acid from the sarcoplasmic reticulum of mouse skeletal muscle fibres. (nih.gov)
- 7. Effect of the organic Ca2+ channel blocker D-600 on sarcoplasmic reticulum Ca2+ uptake in skeletal muscle. (nih.gov)
- 8. The SH3 and cysteine-rich domain 3 (Stac3) gene is important to growth, fiber composition, and calcium release from the sarcoplasmic reticulum in postnatal skeletal muscle. (nih.gov)
- 14. Effects of dantrolene and its derivatives on Ca(2+) release from the sarcoplasmic reticulum of mouse skeletal muscle fibres. (nih.gov)
- In skeletal muscle, Dantrium dissociates the excitation-contraction coupling, probably by interfering with the release of Ca++ from the sarcoplasmic reticulum. (nih.gov)
- Electron microscopy image of a mitochondrion with a donut hole (cyan) as well as sarcoplasmic reticulum (magenta), transverse tubules (orange), and contractile A-bands (green), I-bands (red), and Z-disks (blue) from a mouse glycolytic skeletal muscle. (nih.gov)
- Normal cardiac contraction depends on the maintenance of calcium cycling and homeostasis across the mitochondrial membrane and sarcoplasmic reticulum during each cardiac cycle. (medscape.com)
- Inhibition of calcium release from the sarcoplasmic reticulum by Dantrium reestablishes the myoplasmic calcium equilibrium, increasing the percentage of bound calcium. (nih.gov)
- The sarcoplasmic reticulum provides the intracellular storage and release of calcium required for contraction to occur. (medscape.com)
- The electrical signals conducted by the T-tubules stimulate the sarcoplasmic reticulum to release calcium. (medscape.com)
- Heart muscle contraction is normally activated by a synchronized Ca release from sarcoplasmic reticulum (SR), a major intracellular Ca store. (nih.gov)
- Here, we report that nanomolar concentrations of EGCG significantly enhance contractility of intact murine myocytes by increasing electrically evoked Ca(2+) transients, sarcoplasmic reticulum (SR) Ca(2+) content, and ryanodine receptor type 2 (RyR2) channel open probability. (nih.gov)