Receptor Aggregation
Receptors, Cholinergic
Agrin
Receptors, IgE
Leukemia, Basophilic, Acute
Mast Cells
Cell Aggregation
Cell Membrane
Protein-Tyrosine Kinases
Tyrosine
Signal Transduction
Phosphorylation
Cells, Cultured
Platelet Aggregation Inhibitors
Erythrocyte Aggregation
Blood Platelets
Adenosine Diphosphate
Platelet Activation
Amyloid
Clustering of AMPA receptors by the synaptic PDZ domain-containing protein PICK1. (1/499)
Synaptic clustering of neurotransmitter receptors is crucial for efficient signal transduction and integration in neurons. PDZ domain-containing proteins such as PSD-95/SAP90 interact with the intracellular C termini of a variety of receptors and are thought to be important in the targeting and anchoring of receptors to specific synapses. Here, we show that PICK1 (protein interacting with C kinase), a PDZ domain-containing protein, interacts with the C termini of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptors in vitro and in vivo. In neurons, PICK1 specifically colocalizes with AMPA receptors at excitatory synapses. Furthermore, PICK1 induces clustering of AMPA receptors in heterologous expression systems. These results suggest that PICK1 may play an important role in the modulation of synaptic transmission by regulating the synaptic targeting of AMPA receptors. (+info)Metabolic stabilization of muscle nicotinic acetylcholine receptor by rapsyn. (2/499)
Although the metabolic half-life of muscle endplate acetylcholine receptor (AChR) changes during development and after denervation in the adult, little is known about the molecular mechanisms that influence receptor stability. We have investigated the effect on AChR turnover of its interaction with rapsyn, a 43 kDa peripheral membrane protein that is closely associated with the AChR in muscle cells and is required for its clustering at endplates. Both in transfected COS cells and in cultured myotubes from rapsyn-negative and rapsyn-positive mice, we have found that the presence of rapsyn slows the turnover of AChRs by as much as twofold. The effect was similar for both embryonic (alpha2betadeltagamma) and adult (alpha2betadeltaepsilon) AChRs and for AChRs whose beta subunit lacked a putative tyrosine phosphorylation site. Neither colchicine nor cytochalasin D altered AChR turnover or prevented the rapsyn effect. Mutant rapsyn proteins whose N-terminal myristoylation signal was eliminated, or whose C terminus or zinc-finger domains were deleted, failed to change the rate of receptor turnover. Each of these mutations affects the association of the AChR with rapsyn, suggesting that AChR stability is altered by interaction between the two proteins. Our results suggest that, in addition to its role in AChR clustering, rapsyn also functions to metabolically stabilize the AChR. (+info)Variability of neurotransmitter concentration and nonsaturation of postsynaptic AMPA receptors at synapses in hippocampal cultures and slices. (3/499)
To understand the elementary unit of synaptic communication between CNS neurons, one must know what causes the variability of quantal postsynaptic currents and whether unitary packets of transmitter saturate postsynaptic receptors. We studied single excitatory synapses between hippocampal neurons in culture. Focal glutamate application at individual postsynaptic sites evoked currents (I(glu)) with little variability compared with quantal excitatory postsynaptic currents (EPSCs). The maximal I(glu) was >2-fold larger than the median EPSC. Thus, variations in [glu]cleft are the main source of variability in EPSC size, and glutamate receptors are generally far from saturation during quantal transmission. This conclusion was verified by molecular antagonism experiments in hippocampal cultures and slices. The general lack of glutamate receptor saturation leaves room for increases in [glu]cleft as a mechanism for synaptic plasticity. (+info)CD5 negatively regulates the T-cell antigen receptor signal transduction pathway: involvement of SH2-containing phosphotyrosine phosphatase SHP-1. (4/499)
The negative regulation of T- or B-cell antigen receptor signaling by CD5 was proposed based on studies of thymocytes and peritoneal B-1a cells from CD5-deficient mice. Here, we show that CD5 is constitutively associated with phosphotyrosine phosphatase activity in Jurkat T cells. CD5 was found associated with the Src homology 2 (SH2) domain containing hematopoietic phosphotyrosine phosphatase SHP-1 in both Jurkat cells and normal phytohemagglutinin-expanded T lymphoblasts. This interaction was increased upon T-cell receptor (TCR)-CD3 cell stimulation. CD5 co-cross-linking with the TCR-CD3 complex down-regulated the TCR-CD3-increased Ca2+ mobilization in Jurkat cells. In addition, stimulation of Jurkat cells or normal phytohemagglutinin-expanded T lymphoblasts through TCR-CD3 induced rapid tyrosine phosphorylation of several protein substrates, which was substantially diminished after CD5 cross-linking. The CD5-regulated substrates included CD3zeta, ZAP-70, Syk, and phospholipase Cgammal but not the Src family tyrosine kinase p56(lck). By mutation of all four CD5 intracellular tyrosine residues to phenylalanine, we found the membrane-proximal tyrosine at position 378, which is located in an immunoreceptor tyrosine-based inhibitory (ITIM)-like motif, crucial for SHP-1 association. The F378 point mutation ablated both SHP-1 binding and the down-regulating activity of CD5 during TCR-CD3 stimulation. These results suggest a critical role of the CD5 ITIM-like motif, which by binding to SHP-1 mediates the down-regulatory activity of this receptor. (+info)Globular domains of agrin are functional units that collaborate to induce acetylcholine receptor clustering. (5/499)
Agrin, an extracellular matrix protein involved in neuromuscular junction formation, directs clustering of postsynaptic molecules, including acetylcholine receptors (AChRs). This activity resides entirely in the C-terminal portion of the protein, which consists of three laminin-like globular domains (G-domains: G1, G2 and G3) and four EGF-like repeats. Additionally, alternate mRNA splicing yields G-domain variants G2(0,4) with 0- or 4-amino-acid inserts, and G3(0, 8,11,19) with 0-, 8-, 11- or 19-amino-acid inserts. In order to better understand the contributions of individual domains and alternate splicing to agrin activity, single G-domains and covalently linked pairs of G-domains were expressed as soluble proteins and their AChR clustering activity measured on cultured C2 myotubes. These analyses reveal the following: (1) While only G3(8) exhibits detectable activity by itself, all G-domains studied (G1, G2(0), G2(4), G3(0) and G3(8)) enhance G3(8) activity when physically linked to G3(8). This effect is most pronounced when G2(4) is linked to G3(8) and is independent of the order of the G-domains. (2) The deletion of EGF-like repeats enhances activity. (3) Increasing the physical separation between linked G1 and G3(8) domains produces a significant increase in activity; similar alterations to linked G2 and G3(8) domains are without effect. (4) Clusters induced by two concatenated G3(8) domains are significantly smaller than all other agrin forms studied. These data suggest that agrin G-domains are the functional units which interact independently of their specific organization to yield AChR clustering. G-domain synergism resulting in biological output could be due to physical interactions between G-domains or, alternatively, independent interactions of G-domains with cell surface receptors which require spatially localized coactivation for optimal signal transduction. (+info)Differential roles of N- and C-terminal immunoreceptor tyrosine-based inhibition motifs during inhibition of cell activation by killer cell inhibitory receptors. (6/499)
Killer cell inhibitory receptors (KIRs) inhibit NK and T cell cytotoxicity when recognizing MHC class I molecules on target cells. They possess two tandem intracytoplasmic immunoreceptor tyrosine-based inhibition motifs (ITIMs) that, when phosphorylated, each bind to the two Src homology 2 domain-bearing protein tyrosine phosphatases SHP-1 and SHP-2 in vitro. Using chimeric receptors having an intact intracytoplasmic KIR domain bearing both ITIMs (N + C-KIR), a deleted domain containing the N-terminal ITIM only (N-KIR), or a deleted domain containing the C-terminal ITIM only (C-KIR), we examined the respective contributions of the two ITIMs in the inhibition of cell activation in two experimental models (a rat mast cell and a mouse B cell line) that have been widely used to analyze KIR functions. We found that the two KIR ITIMs play distinct roles. When coaggregated with immunoreceptor tyrosine-based activation motif-bearing receptors such as high-affinity IgE receptors or B cell receptors, the N + C-KIR and the N-KIR chimeras, but not the C-KIR chimera, inhibited mast cell and B cell activation, became tyrosyl-phosphorylated, and recruited phosphatases in vivo. The N + C-KIR chimera recruited SHP-1 as expected, but also SHP-2. Surprisingly, the N-KIR chimera failed to recruit SHP-1; however, it did recruit SHP-2. Consequently, the N-terminal ITIM is sufficient to recruit SHP-2 and to inhibit cell activation, whereas the N-terminal and the C-terminal ITIMs are both necessary to recruit SHP-1. The two KIR ITIMs, therefore, are neither mandatory for inhibition nor redundant. Rather than simply amplifying inhibitory signals, they differentially contribute to the recruitment of distinct phosphatases that may cooperate to inhibit cell activation. (+info)Triggering of effector functions on a CD8+ T cell clone upon the aggregation of an activatory CD94/kp39 heterodimer. (7/499)
Some T lymphocytes express the CD94 Ag, which is known to form heterodimers with members of the NKG2 family. We have studied the expression pattern and function of CD94 heterodimers in different alphabeta or gammadelta T cell clones. Most of the CD94+NKG2A- T cells have a low to intermediate expression of CD94 Ag. The cross-linking of the CD94/NKG2 heterodimer in one of these CD8 alphabeta CD94+NKG2A- T cell clones (K14B06) was able to: 1) increase the intracellular concentration of Ca2+, 2) induce the up-regulation of CD25 Ag expression and the secretion of IFN-gamma, and 3) trigger redirected cytotoxicity in a TCR-independent manner. This activatory property was not shared by any other costimulatory molecule expressed by the K14B06 T cell clone, including CD8, CD28, CD45, CD69, or CD2 Ags. The immunoprecipitation of CD94 heterodimer showed a 39-kDa band with a similar m.w. to the activatory heterodimer found on some NK clones. A novel form of the NKG2 family (NKG2H) was identified in K14B06. NKG2H protein represents an alternative spliced form of the NKG2E gene, displaying a charged residue in the transmembrane portion and a cytoplasmic tail that lacks immunoreceptor tyrosine-based inhibitory motifs. The expression of NKG2H in the cell membrane through its association to CD94 and DAP-12 molecules supports that it could form part of the activatory CD94/Kp39 heterodimer present on K14B06 cells. (+info)Cutting edge: recruitment of the CD19/CD21 coreceptor to B cell antigen receptor is required for antigen-mediated expression of Bcl-2 by resting and cycling hen egg lysozyme transgenic B cells. (8/499)
Recruitment of the CD19/CD21 coreceptor is thought to lower the threshold for effective signaling through the B cell Ag receptor. We provide evidence supporting a second role for coreceptor recruitment, and that is to enhance the survival/proliferative potential of the responding B cells. We show that B cell Ag receptor signaling in the absence of coreceptor recruitment induces cellular accumulation of the anti-apoptotic protein Bcl-xL, whereas CD19-mediated signals are required for Bcl-2 accumulation. The expression of both anti-apoptotic proteins correlates with the enhanced responsiveness of both resting and cycling B cells to growth-promoting signals delivered through CD40. These results provide further evidence for the necessity of coreceptor recruitment during Ag-dependent B cell activation and indicate that Ags derived from inflammatory sites function as better thymus-dependent Ags than their counterparts not coated with complement fragments. (+info)Receptor aggregation, also known as receptor clustering or patching, is a process that occurs when multiple receptor proteins, which are typically found dispersed on the cell membrane, come together and form a cluster or aggregate in response to a stimulus. This can occur through various mechanisms such as ligand-induced dimerization, conformational changes, or interactions with intracellular signaling molecules.
Receptor aggregation can lead to changes in receptor function, including increased sensitivity, altered signaling properties, and internalization of the receptors. This process plays an important role in various physiological processes such as cell signaling, immune response, and neuronal communication. However, abnormal receptor aggregation has also been implicated in several diseases, including cancer and neurological disorders.
Cholinergic receptors are a type of receptor in the body that are activated by the neurotransmitter acetylcholine. Acetylcholine is a chemical that nerve cells use to communicate with each other and with muscles. There are two main types of cholinergic receptors: muscarinic and nicotinic.
Muscarinic receptors are found in the heart, smooth muscle, glands, and the central nervous system. They are activated by muscarine, a type of alkaloid found in certain mushrooms. When muscarinic receptors are activated, they can cause changes in heart rate, blood pressure, and other bodily functions.
Nicotinic receptors are found in the nervous system and at the junction between nerves and muscles (the neuromuscular junction). They are activated by nicotine, a type of alkaloid found in tobacco plants. When nicotinic receptors are activated, they can cause the release of neurotransmitters and the contraction of muscles.
Cholinergic receptors play an important role in many physiological processes, including learning, memory, and movement. They are also targets for drugs used to treat a variety of medical conditions, such as Alzheimer's disease, Parkinson's disease, and myasthenia gravis (a disorder that causes muscle weakness).
Agrin is a protein that plays a crucial role in the formation and maintenance of the neuromuscular junction, which is the specialized synapse between motor neurons and muscle fibers. It is produced by the motor neuron and released into the synaptic cleft, where it helps to cluster acetylcholine receptors on the muscle fiber membrane. This clustering of receptors is essential for efficient neuromuscular transmission and normal muscle function.
Agrin is a large heparan sulfate proteoglycan that contains a number of functional domains, including a unique alternatively spliced region that determines its activity in acetylcholine receptor clustering. Mutations in the gene encoding agrin have been associated with certain forms of congenital myasthenic syndrome, a group of inherited disorders characterized by muscle weakness and fatigability.
IgE receptors, also known as Fc epsilon RI receptors, are membrane-bound proteins found on the surface of mast cells and basophils. They play a crucial role in the immune response to parasitic infections and allergies. IgE receptors bind to the Fc region of immunoglobulin E (IgE) antibodies, which are produced by B cells in response to certain antigens. When an allergen cross-links two adjacent IgE molecules bound to the same IgE receptor, it triggers a signaling cascade that leads to the release of mediators such as histamine, leukotrienes, and prostaglandins. These mediators cause the symptoms associated with allergic reactions, including inflammation, itching, and vasodilation. IgE receptors are also involved in the activation of the adaptive immune response by promoting the presentation of antigens to T cells.
Acute basophilic leukemia (ABL) is a rare and aggressive subtype of acute myeloid leukemia (AML), a type of cancer that affects the blood and bone marrow. In ABL, the malignancy originates from the transformation of hematopoietic stem cells into abnormal blast cells, specifically basophils, in the bone marrow. These blasts proliferate rapidly and disrupt normal blood cell production, leading to a significant decrease in functional red and white blood cells and platelets.
The medical definition of acute basophilic leukemia is:
A malignant neoplasm of hematopoietic stem cells characterized by the uncontrolled proliferation and accumulation of immature basophils (basophilic blasts) in the bone marrow, blood, and occasionally other tissues. This rapidly progressing disorder is accompanied by a decline in the production of normal blood cells, resulting in symptoms such as anemia, fatigue, infection, easy bruising, and bleeding. The diagnosis of ABL typically involves bone marrow aspiration and biopsy, cytogenetic analysis, immunophenotyping, and molecular genetic testing to confirm the presence of leukemic blasts and identify specific genetic abnormalities that can inform prognosis and treatment decisions.
Mast cells are a type of white blood cell that are found in connective tissues throughout the body, including the skin, respiratory tract, and gastrointestinal tract. They play an important role in the immune system and help to defend the body against pathogens by releasing chemicals such as histamine, heparin, and leukotrienes, which help to attract other immune cells to the site of infection or injury. Mast cells also play a role in allergic reactions, as they release histamine and other chemicals in response to exposure to an allergen, leading to symptoms such as itching, swelling, and redness. They are derived from hematopoietic stem cells in the bone marrow and mature in the tissues where they reside.
Cell aggregation is the process by which individual cells come together and adhere to each other to form a group or cluster. This phenomenon can occur naturally during embryonic development, tissue repair, and wound healing, as well as in the formation of multicellular organisms such as slime molds. In some cases, cell aggregation may also be induced in the laboratory setting through the use of various techniques, including the use of cell culture surfaces that promote cell-to-cell adhesion or the addition of factors that stimulate the expression of adhesion molecules on the cell surface.
Cell aggregation can be influenced by a variety of factors, including the type and properties of the cells involved, as well as environmental conditions such as pH, temperature, and nutrient availability. The ability of cells to aggregate is often mediated by the presence of adhesion molecules on the cell surface, such as cadherins, integrins, and immunoglobulin-like cell adhesion molecules (Ig-CAMs). These molecules interact with each other and with extracellular matrix components to promote cell-to-cell adhesion and maintain the stability of the aggregate.
In some contexts, abnormal or excessive cell aggregation can contribute to the development of diseases such as cancer, fibrosis, and inflammatory disorders. For example, the aggregation of cancer cells can facilitate their invasion and metastasis, while the accumulation of fibrotic cells in tissues can lead to organ dysfunction and failure. Understanding the mechanisms that regulate cell aggregation is therefore an important area of research with potential implications for the development of new therapies and treatments for a variety of diseases.
The neuromuscular junction (NMJ) is the specialized synapse or chemical communication point, where the motor neuron's nerve terminal (presynaptic element) meets the muscle fiber's motor end plate (postsynaptic element). This junction plays a crucial role in controlling muscle contraction and relaxation.
At the NMJ, the neurotransmitter acetylcholine is released from the presynaptic nerve terminal into the synaptic cleft, following an action potential. Acetylcholine then binds to nicotinic acetylcholine receptors on the postsynaptic membrane of the muscle fiber, leading to the generation of an end-plate potential. If sufficient end-plate potentials are generated and summate, they will trigger an action potential in the muscle fiber, ultimately causing muscle contraction.
Dysfunction at the neuromuscular junction can result in various neuromuscular disorders, such as myasthenia gravis, where autoantibodies attack acetylcholine receptors, leading to muscle weakness and fatigue.
A cell membrane, also known as the plasma membrane, is a thin semi-permeable phospholipid bilayer that surrounds all cells in animals, plants, and microorganisms. It functions as a barrier to control the movement of substances in and out of the cell, allowing necessary molecules such as nutrients, oxygen, and signaling molecules to enter while keeping out harmful substances and waste products. The cell membrane is composed mainly of phospholipids, which have hydrophilic (water-loving) heads and hydrophobic (water-fearing) tails. This unique structure allows the membrane to be flexible and fluid, yet selectively permeable. Additionally, various proteins are embedded in the membrane that serve as channels, pumps, receptors, and enzymes, contributing to the cell's overall functionality and communication with its environment.
Protein-Tyrosine Kinases (PTKs) are a type of enzyme that plays a crucial role in various cellular functions, including signal transduction, cell growth, differentiation, and metabolism. They catalyze the transfer of a phosphate group from ATP to the tyrosine residues of proteins, thereby modifying their activity, localization, or interaction with other molecules.
PTKs can be divided into two main categories: receptor tyrosine kinases (RTKs) and non-receptor tyrosine kinases (NRTKs). RTKs are transmembrane proteins that become activated upon binding to specific ligands, such as growth factors or hormones. NRTKs, on the other hand, are intracellular enzymes that can be activated by various signals, including receptor-mediated signaling and intracellular messengers.
Dysregulation of PTK activity has been implicated in several diseases, such as cancer, diabetes, and inflammatory disorders. Therefore, PTKs are important targets for drug development and therapy.
A muscle is a soft tissue in our body that contracts to produce force and motion. It is composed mainly of specialized cells called muscle fibers, which are bound together by connective tissue. There are three types of muscles: skeletal (voluntary), smooth (involuntary), and cardiac. Skeletal muscles attach to bones and help in movement, while smooth muscles are found within the walls of organs and blood vessels, helping with functions like digestion and circulation. Cardiac muscle is the specific type that makes up the heart, allowing it to pump blood throughout the body.
Tyrosine is an non-essential amino acid, which means that it can be synthesized by the human body from another amino acid called phenylalanine. Its name is derived from the Greek word "tyros," which means cheese, as it was first isolated from casein, a protein found in cheese.
Tyrosine plays a crucial role in the production of several important substances in the body, including neurotransmitters such as dopamine, norepinephrine, and epinephrine, which are involved in various physiological processes, including mood regulation, stress response, and cognitive functions. It also serves as a precursor to melanin, the pigment responsible for skin, hair, and eye color.
In addition, tyrosine is involved in the structure of proteins and is essential for normal growth and development. Some individuals may require tyrosine supplementation if they have a genetic disorder that affects tyrosine metabolism or if they are phenylketonurics (PKU), who cannot metabolize phenylalanine, which can lead to elevated tyrosine levels in the blood. However, it is important to consult with a healthcare professional before starting any supplementation regimen.
Signal transduction is the process by which a cell converts an extracellular signal, such as a hormone or neurotransmitter, into an intracellular response. This involves a series of molecular events that transmit the signal from the cell surface to the interior of the cell, ultimately resulting in changes in gene expression, protein activity, or metabolism.
The process typically begins with the binding of the extracellular signal to a receptor located on the cell membrane. This binding event activates the receptor, which then triggers a cascade of intracellular signaling molecules, such as second messengers, protein kinases, and ion channels. These molecules amplify and propagate the signal, ultimately leading to the activation or inhibition of specific cellular responses.
Signal transduction pathways are highly regulated and can be modulated by various factors, including other signaling molecules, post-translational modifications, and feedback mechanisms. Dysregulation of these pathways has been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.
Phosphorylation is the process of adding a phosphate group (a molecule consisting of one phosphorus atom and four oxygen atoms) to a protein or other organic molecule, which is usually done by enzymes called kinases. This post-translational modification can change the function, localization, or activity of the target molecule, playing a crucial role in various cellular processes such as signal transduction, metabolism, and regulation of gene expression. Phosphorylation is reversible, and the removal of the phosphate group is facilitated by enzymes called phosphatases.
"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.
Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.
It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.
A cell line is a culture of cells that are grown in a laboratory for use in research. These cells are usually taken from a single cell or group of cells, and they are able to divide and grow continuously in the lab. Cell lines can come from many different sources, including animals, plants, and humans. They are often used in scientific research to study cellular processes, disease mechanisms, and to test new drugs or treatments. Some common types of human cell lines include HeLa cells (which come from a cancer patient named Henrietta Lacks), HEK293 cells (which come from embryonic kidney cells), and HUVEC cells (which come from umbilical vein endothelial cells). It is important to note that cell lines are not the same as primary cells, which are cells that are taken directly from a living organism and have not been grown in the lab.
Platelet aggregation inhibitors are a class of medications that prevent platelets (small blood cells involved in clotting) from sticking together and forming a clot. These drugs work by interfering with the ability of platelets to adhere to each other and to the damaged vessel wall, thereby reducing the risk of thrombosis (blood clot formation).
Platelet aggregation inhibitors are often prescribed for people who have an increased risk of developing blood clots due to various medical conditions such as atrial fibrillation, coronary artery disease, peripheral artery disease, stroke, or a history of heart attack. They may also be used in patients undergoing certain medical procedures, such as angioplasty and stenting, to prevent blood clot formation in the stents.
Examples of platelet aggregation inhibitors include:
1. Aspirin: A nonsteroidal anti-inflammatory drug (NSAID) that irreversibly inhibits the enzyme cyclooxygenase, which is involved in platelet activation and aggregation.
2. Clopidogrel (Plavix): A P2Y12 receptor antagonist that selectively blocks ADP-induced platelet activation and aggregation.
3. Prasugrel (Effient): A third-generation thienopyridine P2Y12 receptor antagonist, similar to clopidogrel but with faster onset and greater potency.
4. Ticagrelor (Brilinta): A direct-acting P2Y12 receptor antagonist that does not require metabolic activation and has a reversible binding profile.
5. Dipyridamole (Persantine): An antiplatelet agent that inhibits platelet aggregation by increasing cyclic adenosine monophosphate (cAMP) levels in platelets, which leads to decreased platelet reactivity.
6. Iloprost (Ventavis): A prostacyclin analogue that inhibits platelet aggregation and causes vasodilation, often used in the treatment of pulmonary arterial hypertension.
7. Cilostazol (Pletal): A phosphodiesterase III inhibitor that increases cAMP levels in platelets, leading to decreased platelet activation and aggregation, as well as vasodilation.
8. Ticlopidine (Ticlid): An older P2Y12 receptor antagonist with a slower onset of action and more frequent side effects compared to clopidogrel or prasugrel.
Erythrocyte aggregation, also known as rouleaux formation, is the clumping together of red blood cells (erythrocytes) in a way that resembles a stack of coins. This phenomenon is typically observed under low-shear conditions, such as those found in small blood vessels and capillaries.
The aggregation of erythrocytes is influenced by several factors, including the concentration of plasma proteins, the charge and shape of the red blood cells, and the flow characteristics of the blood. One of the most important proteins involved in this process is fibrinogen, a large plasma protein that can bridge between adjacent red blood cells and cause them to stick together.
Erythrocyte aggregation can have significant effects on blood flow and rheology (the study of how blood flows), particularly in diseases such as diabetes, sickle cell disease, and certain types of anemia. Increased erythrocyte aggregation can lead to reduced oxygen delivery to tissues, increased blood viscosity, and impaired microcirculatory flow, all of which can contribute to tissue damage and organ dysfunction.
Blood platelets, also known as thrombocytes, are small, colorless cell fragments in our blood that play an essential role in normal blood clotting. They are formed in the bone marrow from large cells called megakaryocytes and circulate in the blood in an inactive state until they are needed to help stop bleeding. When a blood vessel is damaged, platelets become activated and change shape, releasing chemicals that attract more platelets to the site of injury. These activated platelets then stick together to form a plug, or clot, that seals the wound and prevents further blood loss. In addition to their role in clotting, platelets also help to promote healing by releasing growth factors that stimulate the growth of new tissue.
Adenosine diphosphate (ADP) is a chemical compound that plays a crucial role in energy transfer within cells. It is a nucleotide, which consists of a adenosine molecule (a sugar molecule called ribose attached to a nitrogenous base called adenine) and two phosphate groups.
In the cell, ADP functions as an intermediate in the conversion of energy from one form to another. When a high-energy phosphate bond in ADP is broken, energy is released and ADP is converted to adenosine triphosphate (ATP), which serves as the main energy currency of the cell. Conversely, when ATP donates a phosphate group to another molecule, it is converted back to ADP, releasing energy for the cell to use.
ADP also plays a role in blood clotting and other physiological processes. In the coagulation cascade, ADP released from damaged red blood cells can help activate platelets and initiate the formation of a blood clot.
Platelet activation is the process by which platelets (also known as thrombocytes) become biologically active and change from their inactive discoid shape to a spherical shape with pseudopodia, resulting in the release of chemical mediators that are involved in hemostasis and thrombosis. This process is initiated by various stimuli such as exposure to subendothelial collagen, von Willebrand factor, or thrombin during vascular injury, leading to platelet aggregation and the formation of a platelet plug to stop bleeding. Platelet activation also plays a role in inflammation, immune response, and wound healing.
Amyloid is a term used in medicine to describe abnormally folded protein deposits that can accumulate in various tissues and organs of the body. These misfolded proteins can form aggregates known as amyloid fibrils, which have a characteristic beta-pleated sheet structure. Amyloid deposits can be composed of different types of proteins, depending on the specific disease associated with the deposit.
In some cases, amyloid deposits can cause damage to organs and tissues, leading to various clinical symptoms. Some examples of diseases associated with amyloidosis include Alzheimer's disease (where amyloid-beta protein accumulates in the brain), systemic amyloidosis (where amyloid fibrils deposit in various organs such as the heart, kidneys, and liver), and type 2 diabetes (where amyloid deposits form in the pancreas).
It's important to note that not all amyloid deposits are harmful or associated with disease. However, when they do cause problems, treatment typically involves managing the underlying condition that is leading to the abnormal protein accumulation.
Protein folding is the process by which a protein molecule naturally folds into its three-dimensional structure, following the synthesis of its amino acid chain. This complex process is determined by the sequence and properties of the amino acids, as well as various environmental factors such as temperature, pH, and the presence of molecular chaperones. The final folded conformation of a protein is crucial for its proper function, as it enables the formation of specific interactions between different parts of the molecule, which in turn define its biological activity. Protein misfolding can lead to various diseases, including neurodegenerative disorders such as Alzheimer's and Parkinson's disease.
Cholesterol signaling
Michelle Wang
Rhodopsin
CpG oligodeoxynucleotide
Platelet
Terutroban
Testosterone
CD84
Physiological agonism and antagonism
Tight junction proteins
Non-catalytic tyrosine-phosphorylated receptor
Ticagrelor
Epidermal growth factor receptor
Adenosine diphosphate receptor inhibitor
LIPID MAPS
N-Formylmethionine
Nicergoline
Thromboregulation
Lysenin
Mohammad Zahid Ashraf
Prostaglandin E2
Prasugrel
T-cell receptor
Ligand-dependent nuclear receptor-interacting factor 1
GPR37
Agrin
Adenosine diphosphate
Prostaglandin
Salmon shark
Disintegrin
L-type calcium channels mediate acetylcholine receptor aggregation on cultured muscle
Protease activated receptor-1 (PAR-1) mediated platelet aggregation is dependent on clopidogrel response
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Triggering of the high-affinity IgE receptor in an aggregation-independent manner - CAMS Oxford Institute
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PAR-13-049: Drug Discovery for Nervous System Disorders (R21)
Estrogen-related receptor gamma regulates mitochondrial and synaptic genes and modulates vulnerability to synucleinopathy | npj...
CHRNA5 cholinergic receptor nicotinic alpha 5 subunit [Homo sapiens (human)] - Gene - NCBI
Frontiers | Platelet Membrane Receptor Proteolysis: Implications for Platelet Function
Platelet Activation and Aggregation Induced by Streptococcus bovis/Streptococcus equinus Complex | Lund University Publications
JCI - Sex differences in thrombosis in mice are mediated by sex-specific growth hormone secretion patterns
IUCr) Protein-lipid architecture of a cholinergic postsynaptic membrane
Universitat Jaume I
Christopher W Cairo - Google Scholar
M1 Muscarinic Receptors-Muscling APP to a Better End? | ALZFORUM
Frontiers | An altered transcriptome underlies cln5-deficiency phenotypes in Dictyostelium discoideum
Platelet Disorders: Overview of Platelet Disorders, Pathophysiology of Platelet Disorders, Autoimmune Thrombocytopenias
Rapid Detection of Tebuconazole Based on Aptasensor and Aggregation of Silver Nanoparticles
Platelets13
- While most studies to date have focused on the effects of this receptor in platelets, PEAR1 is located in multiple tissues including the endothelium, where it is most highly expressed. (duke.edu)
- Platelets and serum were treated with different inhibitors to determine mechanisms involved in platelet aggregation and activation. (lu.se)
- It adds SBSEC to a group of bacteria that activate and aggregate platelets via the platelet Fc-receptor. (lu.se)
- The activities of adhesion and signaling receptors in platelets are controlled by several mechanisms. (frontiersin.org)
- The proteases involved are of different origins and types: (i) present as precursor in plasma, (ii) secreted into the plasma by activated platelets or other blood cells, or (iii) intracellularly activated and cleaving cytosolic receptor domains. (frontiersin.org)
- The flow-dependent adhesion of platelets to those and other extracellular matrix components is stabilized by a panel of integrins, including integrin α 2 β 1 , α IIb β 3 , and α 6 β 1 (adhesive platelet population), while the initial activation of platelets is achieved by signaling via the collagen/laminin receptor, glycoprotein VI (GPVI). (frontiersin.org)
- Although these platelet activation processes are relatively well-studied as a function of the platelet environment, only since recently it is becoming clear that a multitude of proteases present in plasma or produced by platelets themselves are important for the distinct properties of platelet populations, often by cleaving specific receptors. (frontiersin.org)
- CD41/CD61 is expressed on platelets and megakaryocytes, and plays a role in platelet activation and aggregation through interaction with fibrinogen, fibronectin, vWF, and other RGD-containing adhesion molecules. (biolegend.com)
- Platelets express the receptors for adiponectin. (cun.es)
- In its active form, clopidogrel prevents (inhibits) the function of a receptor protein known as P2RY12 that is found on the surface of platelets. (medlineplus.gov)
- the P2RY12 receptor protein helps platelets cluster together to form a clot to seal off damaged blood vessels and prevent blood loss. (medlineplus.gov)
- During activation, platelets release mediators of aggregation, including adenosine diphosphate (ADP) from storage granules. (msdmanuals.com)
- ADP, thromboxane A2, and other mediators induce activation and aggregation of additional platelets on the injured endothelium. (msdmanuals.com)
Acetylcholine7
- Regulation of agrin-induced acetylcholine receptor aggregation by Ca++ and phorbol ester. (rupress.org)
- The aim of the studies reported here was to characterize the effects of agrin on the distribution of acetylcholine receptors (AChRs) and cholinesterase as a step toward determining agrin's mechanism of action. (rupress.org)
- The protein encoded by this gene is a nicotinic acetylcholine receptor subunit and a member of a superfamily of ligand-gated ion channels that mediate fast signal transmission at synapses. (nih.gov)
- Activation of muscarinic acetylcholine receptors is known to steer APP down the non-amyloidogenic, α-secretase pathway, but it has been difficult to pin the effect on a specific receptor subtype: There are five different muscarinic receptors (M1-M5) and knowing which one is involved is critical for making selective drugs and minimizing cholinergic side effects. (alzforum.org)
- The muscarinic acetylcholine receptor has been a target for AD therapies for decades, based first on the loss of acetylcholine in the disease and the role of M1 receptors in memory and cognition, and then on the finding that the receptors control the processing of amyloid precursor protein to Aβ peptides. (alzforum.org)
- They show that treating cultured mouse neurons expressing human APP with the acetylcholine receptor agonist carbachol increased the production of α-secretase cleavage products, but no such effect occurred in cells from M1 knockout mice. (alzforum.org)
- Most notably, Agrin is responsible for the clustering of acetylcholine receptors (AChRs) on the cell surface and their localization to the neuromuscular junction. (thermofisher.com)
Agrin-induced AChR aggregation3
- Although the agrin/MuSK signaling pathway remains largely unknown, changes in intracellular calcium levels are required for agrin-induced AChR aggregation (Megeath and Fallon [1998]: J Neurosci 18: 672-678). (nih.gov)
- Blockade of L-CaChs in muscle cultures inhibited agrin-induced AChR aggregation but not tyrosine phosphorylation of MuSK or AChR beta subunits. (nih.gov)
- The formation and maintenance of agrin-induced AChR aggregates required Ca++, Co++ and Mn++ inhibited agrin-induced AChR aggregation and increased the rate of aggregate dispersal. (rupress.org)
High-affinity IgE receptor1
- Fc[epsilon]RI , the high affinity IgE receptor, is the primary receptor on mast cells. (igert.org)
Agonist4
- Platelet aggregation was measured in 55 patients undergoing elective PCI at 16-24 hours after 600 mg clopidogrel loading dose by light transmittance aggregometry using ADP 20 μM and thrombin receptor agonist peptide (TRAP) at 15 μM and 25 μM as agonists. (nih.gov)
- Betahistine hydrochloride is a histamine H1 receptor agonist that can resist platelet aggregation. (ijpsonline.com)
- Betahistine hydrochloride is a Histamine (H 1 ) receptor agonist that can resist platelet aggregation. (ijpsonline.com)
- Here, we observed that HDL isolated from healthy individuals inhibited the production of inflammatory cytokines by peripheral monocytes stimulated with a Toll-like receptor 2 agonist. (lww.com)
Blockade3
- We developed a calcium signaling-based assay, using cultured human embryonic kidney cells (HEK), that evaluates simultaneously, the activation/desensitization or blockade of the proteinase-activated receptors, PAR 1 and PAR 2 . (aspetjournals.org)
- This study suggests nstpbp5185, an orally selective antithrombotic agent, acting through blockade of TXA2 receptor, may be efficacious for prevention or treatment of pathologic thrombosis. (tmu.edu.tw)
- Blockade of the platelet Fc-receptor or enzymatic cleavage of IgG abolished platelet activation and aggregation. (lu.se)
Thrombin5
- Thrombin induces platelet aggregation by binding to protease activated receptor-1 (PAR-1), and inhibition of PAR-1 has been evaluated in patients treated with clopidogrel to reduce ischemic events after acute coronary syndromes. (nih.gov)
- Furthermore, we used this assay to develop a PAR 1 receptor-activating probe [Ala-parafluoroPhe-Arg-Cha-Cit-Tyr-NH 2 (Cit-NH 2 )], which displays a high degree of specificity for PAR 1 over PAR 2 , and we used the assay to quantitate the ability of trypsin to disarm the activation of PAR 1 by thrombin. (aspetjournals.org)
- In contrast, thrombin receptor-activating peptides derived from the human PAR 1 receptor sequence (e.g. (aspetjournals.org)
- Figure 2: Platelet aggregation induced shear microgradients occurs independently of ADP, TXA 2 and thrombin. (nature.com)
- inhibits thrombin TRAP-6-induced platelet aggregation (IC 50 = 2.5 μ M) with no effect on coagulation time. (tocris.com)
Inhibits2
Human platelet aggregation2
- The abilities of the PAR 1 -targeted agents to desensitize or block PAR 1 in the HEK cell assay were compared with their activities in a human platelet aggregation assay. (aspetjournals.org)
- Nstpbp5185 concentration-dependently inhibited human platelet aggregation caused by collagen, arachidonic acid and U46619. (tmu.edu.tw)
Inhibition1
- Stimulation of postsynaptic GABA B receptors generally triggers inhibition of adenylate cyclase and activation of G protein-gated inwardly rectifying K + (GIRK/Kir3) channels, leading to cell hyperpolarisation (Kaupmann et al. (springer.com)
Cholinergic2
- The cholinergic postsynaptic membrane is an acetyl-choline receptor-rich membrane mediating fast chemical communication at the nerve-muscle synapse. (iucr.org)
- Selectivity is important on both counts: Non-specific muscarinic receptor agonists can produce side effects due to peripheral cholinergic effects including gastrointestinal disturbances, changes in blood pressure, and excessive sweating. (alzforum.org)
P2Y122
- Upon administration, bentracimab binds to free ticagrelor so that ticagrelor cannot bind to the P2Y12 platelet receptor. (the-hospitalist.org)
- Platelet receptors for ADP include the P2Y12 receptor, which sends signals to suppress adenylate cyclase, decreases cyclic adenosine monophosphate (cAMP) levels, and promotes activation of the glycoprotein IIb/IIIa receptor (assembled on the activated platelet surface membrane from glycoproteins IIb and IIIa). (msdmanuals.com)
AChRs2
- Here, we show that L-type calcium channels (L-CaChs) are required for full agrin-induced aggregation of AChRs and sufficient to induce agrin-independent AChR aggregation. (nih.gov)
- Our results establish a novel role for L-CaChs as important sources of the intracellular calcium necessary for the aggregation of AChRs. (nih.gov)
Tyrosine kinase1
- Interestingly, a unique receptor tyrosine kinase, designated MuSK, has been discovered that interacts with Agrin and is specifically localized to developing muscle. (thermofisher.com)
Platelet rich1
- The collagen-induced platelet aggregation of platelet-rich plasma samples from 14 healthy rabbits was measured turbidometrically using a platelet aggregometer, before and 1 hour after intravenous injection of alum. (who.int)
Protease-activate2
- Sex-specific platelet activation through protease-activated receptor-1 in patients undergoing cardiac catheterization. (harvard.edu)
- FR 171113 is a protease-activated receptor 1 (PAR 1 ) antagonist. (tocris.com)
Promote platelet1
- Without active clopidogrel to interfere, the P2RY12 receptor continues to promote platelet aggregation and blood clot formation, which can lead to heart attacks, strokes, and thromboses in individuals with a history of these conditions. (medlineplus.gov)
Ligand1
- Our structural and functional assays demonstrate the different binding modes of chemically distinct agonists of S1PRs, reveal the mechanical switch that activates these receptors, and provide a framework for understanding ligand selectivity and G protein coupling. (rcsb.org)
Membrane9
- Platelet Endothelial Aggregation Receptor 1 (PEAR1) is a newly identified membrane protein reported to be involved in multiple vascular and thrombotic processes. (duke.edu)
- Figure 5: Stabilized discoid platelet aggregation occurs via restructuring of membrane tethers. (nature.com)
- An atomic model, obtained by fitting crystal structures of diferric Tf and the receptor ectodomain into the map, shows that the Tf N-lobe is sandwiched between the membrane and the TfR ectodomain and that the C-lobe abuts the receptor helical domain. (rcsb.org)
- Here, we review current knowledge how proteases act on platelet receptors and the platelet membrane surface. (frontiersin.org)
- Cholesterol interactions with the receptor are apparently essential for stabilizing and maintaining its physiological architecture, since the transmembrane structure contracts, involving displacements of the helices at the outer membrane surface by ∼2 Å (1-3 Å), when this lipid is extracted. (iucr.org)
- Structure of the ACh receptor in Torpedo postsynaptic membrane. (iucr.org)
- Platelet membrane glycoprotein complex important for platelet adhesion and aggregation. (harvard.edu)
- SPT of QD-IgE on live cells combined with the quantification of receptor mobility using the maximum likelihood estimator for diffusion will provide significant insights into membrane protein dynamics. (igert.org)
- VWF binds to receptors on the platelet surface membrane (glycoprotein Ib/IX). (msdmanuals.com)
Mediate2
- Metabotropic GABA B receptors mediate slow inhibitory effects presynaptically and postsynaptically through the modulation of different effector signalling pathways. (springer.com)
- GABA B receptors are the G protein-coupled receptors for GABA, the main inhibitory neurotransmitter in the brain, and through coupling to different intracellular signal transduction mechanisms they mediate slow inhibitory postsynaptic potentials (IPSPs) (Bettler et al. (springer.com)
Thrombus formation1
- Savage, B., Almus-Jacobs, F. & Ruggeri, Z.M. Specific synergy of multiple substrate-receptor interactions in platelet thrombus formation under flow. (nature.com)
Induce1
- This study reports that 22 of 26 tested isolates of different subspecies within SBSEC can induce aggregation, and that aggregation is host dependent. (lu.se)
Agonists2
- It has long been assumed that platelet aggregation and thrombus growth are initiated by soluble agonists generated at sites of vascular injury. (nature.com)
- By using high-resolution intravital imaging techniques and hydrodynamic analyses, we show that platelet aggregation is primarily driven by changes in blood flow parameters (rheology), with soluble agonists having a secondary role, stabilizing formed aggregates. (nature.com)
Antagonist1
- Nstpbp5185 caused a right-shift of the concentration-response curve of U46619 and competitively inhibited the binding of3H-SQ-29548 to TP receptor expressed on HEK-293 cells, with an IC50 of 0.1 uM, indicating that nstpbp5185 is a TP antagonist. (tmu.edu.tw)
Binds1
- When Tf binds receptor, its N-lobe moves by about 9 A with respect to its C-lobe. (rcsb.org)
Proteins2
- This phenomenon involves the aggregation of inflammatory proteins. (wikipedia.org)
- Variants of genes encoding TNF receptors and ligands and proteins regulating TNF activation in familial multiple sclerosis. (cdc.gov)
Adhesion1
- In the model organism Dictyostelium discoideum , loss of the CLN5 homolog, cln5 , impacts various cellular and developmental processes including cell proliferation, cytokinesis, aggregation, cell adhesion, and terminal differentiation. (frontiersin.org)
Metabolism1
- Agrin-induced receptor aggregation also was inhibited by phorbol 12-myristate 13-acetate, an activator of protein kinase C, and by inhibitors of energy metabolism. (rupress.org)
Protein8
- Aggregation of beta -amyloid protein (AI? (monash.edu)
- In this study, we investigated the binding of fluorescein-labelled A beta 1-42 (FluoA beta 1-42) to SH-SY5Y neuroblastoma cells and examined the effect of the 39 kDa receptor-associated protein (RAP), on the A beta -cell interaction. (monash.edu)
- Reelin receptors and intracellular adaptor protein Dab1 were found to be necessary for formation of the aggregates. (jneurosci.org)
- To understand the spatial relationship of GABA B receptors with two key effector ion channels, the G protein-gated inwardly rectifying K + (GIRK/Kir3) channel and the voltage-dependent Ca 2+ channel, biochemical and immunohistochemical approaches were performed. (springer.com)
- c ) The 5.8 Å density map and superimposed 2.7 Å structure of the Torpedo receptor (PDB entry 6uwz ) obtained from detergent-solubilized protein complexed with α -bungarotoxin. (iucr.org)
- Applying these to G-Protein Coupled Receptors (GPCRs), which are the single largest family of signaling receptors in human cells. (ucsf.edu)
- Developing computational methods to relate receptors by the similarity of their ligands, rather than by protein sequence or structure. (ucsf.edu)
- It acts as a co-receptor for human immunodeficiency virus (HIV) entry in cells.The protein also has a role in leukocyte chemotaxis. (sigmaaldrich.com)
Vivo3
- Allan Levey and colleagues at Emory University, Atlanta, Georgia, have now used knockout mice to show that the M1 receptor is responsible for regulating APP processing in vivo. (alzforum.org)
- This study investigated the in vivo effect of alum on platelet aggregation and bleeding time in rabbits. (who.int)
- contradiction in the mechanism of action of alum, we evaluated the in vivo effect of Alum (aluminium potassium sulfate) is a alum in terms of collagen-induced platelet food additive and traditional remedy used to aggregation and bleeding time. (who.int)
Clopidogrel4
- Residual PAR-1 mediated platelet aggregation may be dependent on extent of clopidogrel response. (nih.gov)
- Increasing quartiles of 20 μM ADP induced platelet aggregation after clopidogrel loading were associated with increasing levels of TRAP mediated platelet aggregation. (nih.gov)
- Non-responders to clopidogrel show increased residual platelet aggregation induced by TRAP, whereas clopidogrel responders exhibit attenuated response to TRAP. (nih.gov)
- Addition of PAR-1 antiplatelet drugs may be most effective in patients with reduced clopidogrel response and high residual TRAP mediated platelet aggregation. (nih.gov)
Postsynaptic1
- The microdomains may promote cooperativity between neighbouring receptors, leading to an enhanced postsynaptic response. (iucr.org)
Scavenger2
- In contrast, the intestinal SALSA was more enriched with the scavenger receptor cysteine-rich domains. (researchgate.net)
- Finally, MPA-QDs were found to associate with cell surface scavenger receptors, while the THIO-QDs did not. (cdc.gov)
Intracellular1
- We sought to extend the receptor-desensitization paradigm for use with a cultured cell system, in which an intracellular calcium signal rather than a contractile response might be used as an index of receptor activation. (aspetjournals.org)
Genes3
- Previous analyses of dopaminergic (DAergic) neurons from patients with Lewy-body pathology revealed a deficiency in nuclear-encoded genes for mitochondrial respiration, many of which are targets for the transcription factor estrogen-related receptor gamma ( Esrrg /ERRγ). (nature.com)
- in fact, these genes are targets of the transcriptional coactivator and master regulator of transcription of mitochondrial genes peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) 12 . (nature.com)
- Direct regulators of nuclear-encoded mitochondrial genes are members of the estrogen-related receptor (ERR) family, encoded by Esrra , Esrrb and Esrrg . (nature.com)
Mediates2
- SBSEC mediates platelet aggregation in an IgG and IgG-Fc-receptor dependent manner. (lu.se)
- The platelet GP IIb/IIIa complex mediates platelet-to-platelet interactions (platelet aggregation). (medscape.com)
Thrombosis2
- Platelet aggregation at sites of vascular injury is essential for hemostasis and arterial thrombosis. (nature.com)
- Thro-maboxane receptor (TP) is important in vascular physiology, haemostasis and pathophysiological thrombosis. (tmu.edu.tw)
Embryonic1
- 1994. Ah receptor in embryonic mouse palate and effects of TCDD on receptor expression. (cdc.gov)
Activation5
- Aggregation was studied using light-transmission aggregometry and platelet activation using flow cytometry detecting. (lu.se)
- Aggregation was studied using light-transmission aggregometry and platelet activation using flow cytometry detecting surface upregulation of CD62P. (lu.se)
- The Fc-IgG-receptor pathway was shown essential for platelet activation and aggregation. (lu.se)
- To evaluate the association of adiponectin and sCD40L levels with platelet aggregation in the MS and the effects of adiponectin on platelet aggregation and activation. (cun.es)
- Enhanced platelet aggregation and activation markers are found in the metabolic syndrome associated to low adiponectin concentrations. (cun.es)
Mechanisms2
- These findings provide insight into the prothrombotic effects of disturbed blood flow parameters and suggest a fundamental reinterpretation of the mechanisms driving platelet aggregation and thrombus growth. (nature.com)
- Various mechanisms, including endothelial cell nitric oxide and prostacyclin, promote blood fluidity by preventing platelet aggregation and dilating intact blood vessels. (msdmanuals.com)
Collagen1
- Collagen-induced platelet aggregation was significantly reduced after alum injection. (who.int)
Regulates1
- Intercellular calcium communication regulates platelet aggregation and thrombus growth. (nature.com)
Pathway1
- This interrupts one of the key steps in the pathway of platelet aggregation. (the-hospitalist.org)
Selectivity1
- With both receptors present in the same cell, the selectivity or nonselectivity of a variety of compounds that would affect PAR 1 and/or PAR 2 could be efficiently evaluated in a single experiment. (aspetjournals.org)
Therapeutic1
- S1PRs are lipid-sensing receptors and are therapeutic targets for drug development, including potential treatment of COVID-19. (rcsb.org)
Interactions1
- This study indicates that the surface charge and aggregation characteristics of QDs change drastically in biological culture conditions and, in turn, influence nanoparticle and cellular interactions. (cdc.gov)
Cell2
- Furthermore, we reasoned that, provided receptor cross-desensitization did not occur, it would be advantageous to assess PAR-targeted ligands in a cell that expressed both receptors. (aspetjournals.org)
- One example is the aggregation of Fc[epsilon]RI on the cell surface in response to multi-valent antigen. (igert.org)
Cleavage1
- An important way of regulation is provided by proteolytic cleavage of several of these receptors, leading to either a gain or a loss of platelet function. (frontiersin.org)