Articles tagged with Calcium Channels
Scientists have identified a mutation on the CACNA1D gene that affects two families in Pakistan, leading to deafness and an irregular heartbeat. The mutated protein still sits in the cell's surface membrane but fails to open the calcium channel.
Researchers at the University of Calgary have made a breakthrough discovery about how calcium channels regulate neuronal activity. The study reveals that a protein called beta subunit acts as a molecular switch to stabilize or remove calcium channels, controlling excitability in nerve cells.
The Biophysical Society has announced the winners of its 2011 Student Travel Awards, recognizing 11 student researchers for their scientific merit and potential. The awardees will present their research at the 55th Annual Meeting in Baltimore, Maryland, and receive a travel grant.
A research team led by Elise Stanley found that N-type Ca2+ channels can trigger neurotransmitter release with a single channel. This discovery sheds light on the molecular basis of neural impulse transmission and has implications for normal brain processing and nervous system disorders.
Researchers at Temple University discovered that STIM1 protein inhibits voltage-operated calcium channels in non-excitable cells, providing a common mechanism for calcium signaling in both types of cells. This finding reveals a crucial role of STIM1 in sensing low calcium levels and activating Orai channels.
Researchers have found a possible new target for fighting cystic fibrosis, exploiting the crosstalk between two chloride ion channels in mucous gland cells. The study suggests that activating one channel could compensate for the lack of CFTR functionality in affected cells.
A new study published in The Journal of General Physiology reveals that HCN channels play a crucial role in regulating heart rate during stress. The research provides insight into the mechanisms behind the 'flight-or-fight' response, offering new understanding of this complex physiological process.
New research reveals the TRPML1 channel plays a crucial role in lysosome function, offering new avenues for treating conditions like ALS and CMT. The findings suggest that activating this channel could help overcome membrane traffic defects caused by disease-causing mutations.
A mutation in the big-conductance potassium ion channel (BK channel) is linked to epilepsy, altering its dynamics and increasing nerve-cell excitability. The mutation makes part of the channel more rigid, allowing it to toggle open more easily.
Dr. Joel Hirsch's research provides new information on how calcium channels work and offers a framework for designing drugs that can modulate them to provide relief from chronic pain. The discovery has the potential to lead to new treatments for conditions such as backaches, sore limbs, and arthritis.
Johns Hopkins researchers discovered that a tail module in a calcium channel protein controls its sensitivity to calcium, potentially leading to neurodegenerative diseases. This finding has implications for conditions like schizophrenia, Alzheimer's, Parkinson's, and Huntington's.
Researchers at The Johns Hopkins University School of Medicine have unveiled the downstream processes of ion channel inactivation. Two studies show that Cav1.3 channels undergo distinct molecular endpoints during Ca2+-dependent and voltage-dependent inactivation, with a 'shield' mechanism repelling lid closure.
Researchers at the University of Calgary have made a groundbreaking discovery linking ion channels to regulate brain electrical activity. The study found that specific ion channels work in tandem with each other to control nerve impulse timing, redefining how neuronal activity is controlled.
UCSF researchers identified a protein called B1N1 that helps the heart contract. This discovery sheds light on how individual heart cells organize to pump blood through the body.
A large-scale population-based study found that specific sub-class of dihydropyridine cardiovascular medications decreased the risk of Parkinson's disease by 26-30%. The study suggests that these medications' ability to cross the blood-brain barrier may be key to their neuroprotective effects.
Researchers have found that calcium channels on the tongue are involved in enhancing flavors when paired with substances like glutathione. The study provides new insight into the biology of taste and could lead to the development of healthier foods with minimal sugar or salt.
N-type channel function is modified by lipids according to new Rittenhouse laboratory findings, supporting the ArA generation hypothesis. The study provides insight into VGCC modulation, shedding light on an oily competition between two hypotheses.
A study published in the Journal of Cell Biology reveals that PIKfyve, a lipid kinase, protects neurons from calcium overload by degrading voltage-gated calcium channels. This mechanism may provide new insights into neurodegenerative disorders such as stroke, Parkinson's disease, and Alzheimer's disease.
Researchers found that increased calcium current density occurs before seizure onset, and remains elevated during seizure susceptibility periods.
A novel gene called Flower was discovered to play a crucial role in vesicle uptake in neurons, allowing for rapid neurotransmission. The gene's corresponding protein is present in synaptic vesicles and enables calcium influx, initiating exocytosis.
Researchers found that an overactive enzyme plays a role in atrial fibrillation, but does not act alone. The study revealed a synergy between the enzyme and a specific calcium channel mutation, which is necessary for arrhythmia development.
A study published in the Journal of Neuroscience found that a specific gene can be 'switched on' in animals without a genetic predisposition to epilepsy, leading to changes in calcium channels and brain activity. This discovery may reveal a new mechanism for how epilepsy develops in some individuals.
Researchers have discovered a potential treatment for Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT), a rare inherited heart disorder that causes sudden cardiac deaths. Flecainide, a drug used to treat heart arrhythmias, has been found to reduce calcium release in heart cells, counteracting the cause of CPVT.
Researchers from the University of Iowa have discovered that calmodulin kinase II contributes to arrhythmia in Timothy syndrome, a rare disease affecting only 20 people worldwide. Inhibiting this enzyme can prevent irregular heartbeats.
Researchers found that calmodulin uses two lobes to sense local and global calcium levels, allowing it to detect fluctuations within cells. This discovery sheds light on the universal means of communication in cells and has implications for understanding neural diseases.
Scientists have created the first three-dimensional view of the protein TRPV1, which senses the heat of hot peppers and pain. The study reveals surprising information about its structure, including a 'hanging basket' area that regulates the channel.
A study of 7,374 participants found that those taking calcium channel blockers for high blood pressure had a lower risk of developing Parkinson's disease. The medication was shown to cut the risk by 23% compared to non-users, but not other high blood pressure medications.
A study of Medicare Part D plans in California and Hawaii found that while there is significant variation in drug formularies, most classes of drugs have at least one widely-covered option. The researchers identified specific drugs with high coverage rates, including generic drugs and some brand-name medications.
Researchers at Brown University have identified a critical pain pathway that explains why opioids are effective in blocking pain signals. By understanding how these channels work, drug companies can develop more effective painkillers.
Researchers have identified CatSper as a crucial channel facilitating calcium ion entry into sperm tails, enabling hyperactivation and motility. This breakthrough enables direct testing of modulators to block CatSper, potentially leading to the development of a male contraceptive.
Researchers at Jefferson Medical College provide evidence for the conventional theory of voltage-gated ion channel operation. They used a molecular tape measure with high resolution to show that the field through which the voltage sensor's charges moved is very short, lending support to the conventional model.
Researchers at the University of Virginia Health System have identified a new type of pain-sensing neuron in rats, which may serve as a target for future therapies to treat neuropathic pain. The T-type calcium channels in these cells may act as a volume control for pain impulses.
Diabetics with hypertension can significantly reduce cardiovascular disease risks by taking diuretics, according to a new study. The medication has been shown to be more protective against heart failure and stroke in patients with diabetes and high blood pressure.
Raw garlic activates TRPV1 and TRPA1 ion channel proteins in pain-sensing neurons, detecting temperature and pain. The loss of allicin when garlic is cooked accounts for the change in pungency.
Researchers at Johns Hopkins Medicine have identified two proteins that help replace calcium-allowing channels with ones that keep calcium out, potentially protecting nerve cells from Lou Gehrig's disease. The discovery may lead to new ways to harness the channel-changing ability in other brain cells.
Researchers found that diuretics plus calcium channel blockers doubled CVD death risk compared to diuretics plus beta-blockers. Monotherapy with calcium channel blockers also increased CVD death risk by 55%.
Researchers have found that a protein in brain waves is disrupted by chronic alcohol use, leading to sleep problems. This suggests new medications may improve sleep in chronic alcohol users and enhance addiction treatment outcomes.
Scientists discovered how neurons communicate by removing a specific part of the calcium channel molecule, disrupting neurotransmitter release. The study, published in PNAS, sheds light on the fundamental process of neural communication, providing insight into cellular structure and function.
Researchers have identified a rare genetic syndrome, Timothy syndrome, characterized by cardiac arrhythmias and atypical autism. The syndrome arises from a single gene mutation that impairs a fundamental calcium channel, leading to widespread cellular overloading. Calcium-channel blocking drugs may provide treatment for symptoms.
Timothy syndrome is caused by spontaneous genetic mutations that interfere with calcium channels regulating heart excitation and contraction. A class of drugs may alleviate arrhythmia, while improving cognitive function in some cases. The disorder affects 200,000 to 400,000 children in the US.
Using guinea pigs, researchers increased production of G-protein Gem, which decreased calcium current densities by 30-90% and helped steady irregular heartbeats. Gene therapy shows promise as an alternative to calcium channel blockers with fewer side effects.
Researchers have found a new therapeutic target for stroke by blocking calcium-permeable AMPA receptors, which cause neuronal death. Introducing a form of GluR2 that renders AMPA receptors impermeable to calcium protects vulnerable neurons from ischemia.
Researchers created a mouse model for migraines to study debilitating headaches. The FHM mouse showed increased calcium channel activation and susceptibility to cortical spreading depression (CSD), suggesting hyperexcitability in the brain may trigger pain.
Researchers found that T-type calcium channels are essential for normal nitric oxide-controlled relaxation, and their loss leads to constricted coronary arteries. The study provides insight into the role of this channel in coronary artery relaxation and may lead to new therapeutic targets.
Researchers discovered that mice lacking calcium channels exhibit constricted coronary arteries and fibrous tissue in their hearts, suggesting a potential target for treating cardiovascular disease. The study found that drugs targeting the T-channel, responsible for relaxation, might be used to open arteries.
Researchers have discovered that oral medications commonly used to treat hypertension are also effective in preventing iron overload from causing permanent damage to the heart. The study suggests that these drugs may offer a new treatment option for patients with hereditary hemochromatosis and other genetic disorders
U.Va. researchers have identified T-type calcium channels as a key regulator of low-voltage-activated calcium channels, a crucial process in various cell types. This breakthrough could lead to the development of more specific and effective drugs for cardiovascular diseases.
Researchers found that consuming sesame oil as the sole cooking oil for 60 days lowered patients' blood pressure levels from 166/101 mm Hg to 134/84.6 mm Hg, with a reduced dose of nifedipine from 22.7 mg/day to 7.45 mg/day. The effect may be attributed to polyunsaturated fatty acids and sesamin in sesame oil.
Researchers found that calcium channel blockers primarily affect small arteries called 'store-operated' channels, suggesting a new class of drugs with fewer side effects. This discovery could lead to improved treatment options for heart disease and high blood pressure.
Researchers at Johns Hopkins have discovered that a protein called CNGA4 helps the brain adapt to smells by plugging a channel in odor receptor cells. The study found that mice without this protein can't adapt to odors, and the electrical signal from these neurons stays constant over time.
Researchers at Howard Hughes Medical Institute have developed a new technique to visualize the function of synaptic channels using optical fluctuation analysis. The study revealed that individual synapses typically hold only about six calcium channels, which open with high probability in response to action potentials.
Deleting the b1 subunit of the BK channel in mice causes high blood pressure and enlarged hearts, suggesting it as a promising target for anti-hypertension drugs. The study provides a new model for investigating the molecular basis of hypertension.
Researchers at the University of North Carolina at Chapel Hill have discovered that calcium channels help regulate cell movement by opening to admit more calcium ions when cells are stretched. This boost in motility enables cells to move forward again, which could lead to breakthroughs in wound healing and cancer treatment.
A study found a significant increase in advertising for calcium channel blockers and ACE inhibitors, paralleling a trend away from beta blockers and diuretics. The authors suggest that pharmaceutical marketing efforts may have contributed to this shift, despite scientific evidence favoring the older drugs.
Researchers found that R-type channels control transmitter release in presynaptic terminals, contributing to fine-tuning synaptic activity. These high-voltage-activated channels are resistant to known blockers and have been identified through simultaneous recordings of Ca2+ influx and EPSC evoked by a single action potential.
A study of 6,100 veterans found that diuretics and diuretic plus beta-blocker regimens were the most effective in lowering blood pressure, producing average pressures of 140.1/81.9 mmHg. In contrast, calcium channel blockers had the highest average pressures of 149.0/86.5 mmHg.
Researchers have found a potential link between calcium channel blockers and brain damage, as well as impaired memory. The study analyzed data from the Cardiovascular Health Study and found that participants taking these medications had more evidence of white matter hyperintensity and lower scores on mental tests.
A new analysis linked short-acting calcium channel blockers to a twice increased risk of breast cancer in postmenopausal women. However, longer-acting varieties were not found to have the same association.
A meta-analysis of 98 studies found that sustained-release and extended-release formulations of nifedipine are safe when used in combination with diuretics or beta blockers. However, patients taking short-acting nifedipine were more likely to experience adverse side effects.
High blood pressure can lead to enlargement of heart cells and a silent defect in the heart's pumping mechanism. The researchers found that this defect reduces contraction in each heart cell, contributing to heart failure. Developing novel treatments may be possible with improved understanding of the molecular defects.