Viral Envelope Proteins
Molecular Sequence Data
Platelet Membrane Glycoproteins
Electrophoresis, Polyacrylamide Gel
Amino Acid Sequence
Viral Fusion Proteins
Peptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase
Lysosome-Associated Membrane Glycoproteins
Receptors, Concanavalin A
Wheat Germ Agglutinins
Gene Products, env
Protein Processing, Post-Translational
Herpesvirus 1, Suid
HIV Envelope Protein gp120
Variant Surface Glycoproteins, Trypanosoma
Parainfluenza Virus 1, Human
Fluorescent Antibody Technique
Hemagglutinin Glycoproteins, Influenza Virus
Vesicular stomatitis Indiana virus
HIV Envelope Protein gp41
Receptors, Cell Surface
Blood Group Antigens
HIV Envelope Protein gp160
env Gene Products, Human Immunodeficiency Virus
Viral Structural Proteins
Chromatography, High Pressure Liquid
Lewis Blood-Group System
Recombinant Fusion Proteins
Parainfluenza Virus 3, Human
ABO Blood-Group System
Herpesvirus 1, Bovine
Guanosine Diphosphate Mannose
Herpesvirus 1, Human
Sequence Homology, Amino Acid
Chromatography, Ion Exchange
Cell Adhesion Molecules
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Neu differentiation factor stimulates phosphorylation and activation of the Sp1 transcription factor. (1/19351)Neu differentiation factors (NDFs), or neuregulins, are epidermal growth factor-like growth factors which bind to two tyrosine kinase receptors, ErbB-3 and ErbB-4. The transcription of several genes is regulated by neuregulins, including genes encoding specific subunits of the acetylcholine receptor at the neuromuscular junction. Here, we have examined the promoter of the acetylcholine receptor epsilon subunit and delineated a minimal CA-rich sequence which mediates transcriptional activation by NDF (NDF-response element [NRE]). Using gel mobility shift analysis with an NRE oligonucleotide, we detected two complexes that are induced by treatment with neuregulin and other growth factors and identified Sp1, a constitutively expressed zinc finger phosphoprotein, as a component of one of these complexes. Phosphatase treatment, two-dimensional gel electrophoresis, and an in-gel kinase assay indicated that Sp1 is phosphorylated by a 60-kDa kinase in response to NDF-induced signals. Moreover, Sp1 seems to act downstream of all members of the ErbB family and thus may funnel the signaling of the ErbB network into the nucleus. (+info)
Regulation of neurotrophin-3 expression by epithelial-mesenchymal interactions: the role of Wnt factors. (2/19351)Neurotrophins regulate survival, axonal growth, and target innervation of sensory and other neurons. Neurotrophin-3 (NT-3) is expressed specifically in cells adjacent to extending axons of dorsal root ganglia neurons, and its absence results in loss of most of these neurons before their axons reach their targets. However, axons are not required for NT-3 expression in limbs; instead, local signals from ectoderm induce NT-3 expression in adjacent mesenchyme. Wnt factors expressed in limb ectoderm induce NT-3 in the underlying mesenchyme. Thus, epithelial-mesenchymal interactions mediated by Wnt factors control NT-3 expression and may regulate axonal growth and guidance. (+info)
A novel class of protein from wheat which inhibits xylanases. (3/19351)We have purified a novel class of protein that can inhibit the activity of endo-beta-1,4-xylanases. The inhibitor from wheat (Triticum aestivum, var. Soisson) is a glycosylated, monomeric, basic protein with a pI of 8.7-8.9, a molecular mass of 29 kDa and a unique N-terminal sequence of AGGKTGQVTVFWGRN. We have shown that the protein can inhibit the activity of two family-11 endo-beta-1, 4-xylanases, a recombinant enzyme from Aspergillus niger and an enzyme from Trichoderma viride. The inhibitory activity is heat and protease sensitive. The kinetics of the inhibition have been characterized with the A. niger enzyme using soluble wheat arabinoxylan as a substrate. The Km for soluble arabinoxylan in the absence of inhibitor is 20+/-2 mg/ml with a kcat of 103+/-6 s-1. The kinetics of the inhibition of this reaction are competitive, with a Ki value of 0.35 microM, showing that the inhibitor binds at or close to the active site of free xylanase. This report describes the first isolation of a xylanase inhibitor from any organism. (+info)
Structural characterization of the N-linked oligosaccharides in bile salt-stimulated lipase originated from human breast milk. (4/19351)The detailed structures of N- glycans derived from bile salt-stimulated lipase (BSSL) found in human milk were determined by combining exoglycosidase digestion with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. The N- glycan structures were conclusively determined in terms of complexity and degree of fucosylation. Ion-exchange chromatography with pulsed amperometric detection, together with mass-spectral analysis of the esterified N- glycans, indicated the presence of monosialylated structures. The molecular mass profile of esterified N- glycans present in BSSL further permitted the more detailed studies through collision-induced dissociation (CID) and sequential exoglycosidase cleavages. The N- glycan structures were elucidated to be complex/dibranched, fucosylated/complex/dibranched, monosialylated/complex/dibranched, and monosialylated/fucosylated/dibranched entities. (+info)
Gas-liquid chromatography of the heptafluorobutyrate derivatives of the O-methyl-glycosides on capillary columns: a method for the quantitative determination of the monosaccharide composition of glycoproteins and glycolipids. (5/19351)We have developed a method involving the formation of hepta-fluorobutyrate derivatives of O-methyl-glycosides liberated from glycoproteins and glycolipids following methanolysis. The stable derivatives of the most common monosaccharides of these glycoconjugates (Ara, Rha, Xyl, Fuc, Gal, Man, Glc, GlcNAc, GalNAc, Neu5Ac, KDN) can be separated and quantitatively and reproducibly determined with a high degree of sensitivity level (down to 25 pmol) in the presence of lysine as an internal standard. The GlcNAc residue bound to Asn in N-glycans is quantitatively recovered as two peaks. The latter were easily distinguished from the other GlcNAc residues of N-glycans, thus allowing a considerable improvement of the data on structure of N-glycans obtained from a single carbohydrate analysis. The most common contaminants present in buffers commonly used for the isolation of soluble or membrane-bound glycoproteins (SDS, Triton X-100, DOC, TRIS, glycine, and polyacrylamide or salts, as well as monosaccharide constituents of proteoglycans or degradation products of nucleic acids) do not interfere with these determinations. A carbohydrate analysis of glycoproteins isolated from a SDS/PAGE gel or from PDVF membranes can be performed on microgram amounts without significant interferences. Since fatty acid methyl esters and sphingosine derivatives are separated from the monosaccharide peaks, the complete composition of gangliosides can be achieved in a single step starting from less than 1 microg of the initial compound purified by preparative Silicagel TLC. Using electron impact ionization mass spectrometry, reporter ions for the different classes of O-methyl-glycosides (pentoses, deoxy-hexoses, hexoses, hexosamines, uronic acids, sialic acid, and KDN) allow the identification of these compounds in very complex mixtures. The mass of each compound can be determined in the chemical ionization mode and detection of positive or negative ions. This method presents a considerable improvement compared to those using TMS derivatives. Indeed the heptafluorobutyrate derivatives are stable, and acylation of amino groups is complete. Moreover, there is no interference with contaminants and the separation between fatty acid methyl-esters and O-methyl glycosides is achieved. (+info)
Antiphospholipid, anti-beta 2-glycoprotein-I and anti-oxidized-low-density-lipoprotein antibodies in antiphospholipid syndrome. (6/19351)Antiphospholipid antibodies (aPL), anti-beta 2-glycoprotein I (anti-beta 2-GPI) and anti-oxidized-low-density lipoprotein (LDL) antibodies are all implicated in the pathogenesis of antiphospholipid syndrome. To investigate whether different autoantibodies or combinations thereof produced distinct effects related to their antigenic specificities, we examined the frequencies of antiphospholipid syndrome (APS)-related features in the presence of different antibodies [aPL, beta 2-GPI, anti-oxidized low density lipoprotein (LDL)] in 125 patients with APS. Median follow-up was 72 months: 58 patients were diagnosed as primary APS and 67 as APS plus systemic lupus erythematosus (SLE). Anticardiolipin antibodies (aCL), anti-beta 2-GPI and anti-oxidized LDL antibodies were determined by ELISA; lupus anticoagulant (LA) by standard coagulometric methods. Univariate analysis showed that patients positive for anti-beta 2-GPI had a higher risk of recurrent thrombotic events (OR = 3.64, 95% CI, p = 0.01) and pregnancy loss (OR = 2.99, 95% CI, p = 0.004). Patients positive for anti-oxidized LDL antibodies had a 2.24-fold increase in the risk of arterial thrombosis (2.24, 95% CI, p = 0.03) and lower risk of thrombocytopenia (OR = 0.41 95% CI, p = 0.04). Patients positive for aCL antibodies had a higher risk of pregnancy loss (OR = 4.62 95% CI, p = 0.001). When these data were tested by multivariate logistic regression, the association between anti-beta 2-GPI and pregnancy loss and the negative association between anti-oxidized LDL antibodies and thrombocytopenia disappeared. (+info)
Associations of anti-beta2-glycoprotein I autoantibodies with HLA class II alleles in three ethnic groups. (7/19351)OBJECTIVE: To determine any HLA associations with anti-beta2-glycoprotein I (anti-beta2GPI) antibodies in a large, retrospectively studied, multiethnic group of 262 patients with primary antiphospholipid antibody syndrome (APS), systemic lupus erythematosus (SLE), or another connective tissue disease. METHODS: Anti-beta2GPI antibodies were detected in sera using an enzyme-linked immunosorbent assay. HLA class II alleles (DRB1, DQA1, and DQB1) were determined by DNA oligotyping. RESULTS: The HLA-DQB1*0302 (DQ8) allele, typically carried on HLA-DR4 haplotypes, was associated with anti-beta2GPI when compared with both anti-beta2GPI-negative SLE patients and ethnically matched normal controls, especially in Mexican Americans and, to a lesser extent, in whites. Similarly, when ethnic groups were combined, HLA-DQB1*0302, as well as HLA-DQB1*03 alleles overall (DQB1*0301, *0302, and *0303), were strongly correlated with anti-beta2GPI antibodies. The HLA-DR6 (DR13) haplotype DRB1*1302; DQB1*0604/5 was also significantly increased, primarily in blacks. HLA-DR7 was not significantly increased in any of these 3 ethnic groups, and HLA-DR53 (DRB4*0101) was increased in Mexican Americans only. CONCLUSION: Certain HLA class II haplotypes genetically influence the expression of antibodies to beta2GPI, an important autoimmune response in the APS, but there are variations in HLA associations among different ethnic groups. (+info)
The latrophilin family: multiply spliced G protein-coupled receptors with differential tissue distribution. (8/19351)Latrophilin is a brain-specific Ca2+-independent receptor of alpha-latrotoxin, a potent presynaptic neurotoxin. We now report the finding of two novel latrophilin homologues. All three latrophilins are unusual G protein-coupled receptors. They exhibit strong similarities within their lectin, olfactomedin and transmembrane domains but possess variable C-termini. Latrophilins have up to seven sites of alternative splicing; some splice variants contain an altered third cytoplasmic loop or a truncated cytoplasmic tail. Only latrophilin-1 binds alpha-latrotoxin; it is abundant in brain and is present in endocrine cells. Latrophilin-3 is also brain-specific, whereas latrophilin-2 is ubiquitous. Together, latrophilins form a novel family of heterogeneous G protein-coupled receptors with distinct tissue distribution and functions. (+info)
Some common types of blood platelet disorders include:
1. Thrombocytopenia: This is a condition in which there are too few platelets in the blood. It can be caused by a variety of factors, including autoimmune disorders, bone marrow disorders, and certain medications.
2. Bernard-Soulier syndrome: This is a rare inherited disorder that affects the function of platelets and causes easy bruising and prolonged bleeding.
3. Glanzmann's thrombasthenia: This is a rare inherited disorder that affects the platelets' ability to clot properly, leading to excessive bleeding.
4. Platelet dysfunction: This can be caused by a variety of factors, including certain medications, infections, and autoimmune disorders. It can lead to excessive bleeding or prolonged bleeding after injury or surgery.
5. Congenital amegakaryocytic thrombocytopenia: This is a rare inherited disorder that affects the development of platelets in the bone marrow, leading to a lack of platelets in the blood.
6. Grey platelet syndrome: This is a rare inherited disorder that affects the structure of platelets, making them more prone to rupture and lead to easy bruising and prolonged bleeding.
7. Platelet-type von Willebrand disease: This is a mild bleeding disorder caused by a deficiency of von Willebrand factor, a protein that helps platelets stick together to form clots.
8. acquired platelet dysfunction: This can be caused by various conditions such as infections, medications, and autoimmune disorders.
These disorders can be diagnosed through blood tests, including a complete blood count (CBC) and a platelet function test. Treatment options vary depending on the specific disorder and may include medication, surgery, or lifestyle changes.
Examples of inborn errors of carbohydrate metabolism include:
1. Phosphofructokinase (PFK) deficiency: This is a rare genetic disorder that affects the body's ability to break down glucose-6-phosphate, a type of sugar. Symptoms can include seizures, developmental delays, and metabolic acidosis.
2. Galactosemia: This is a group of genetic disorders that affect the body's ability to process galactose, a type of sugar found in milk and other dairy products. Untreated, galactosemia can lead to serious health problems, including liver disease, kidney damage, and cognitive impairment.
3. Glycogen storage disease type II (GSDII): This is a rare genetic disorder that affects the body's ability to store and use glycogen, a complex carbohydrate found in the liver and muscles. Symptoms can include low blood sugar, fatigue, and muscle weakness.
4. Pompe disease: This is a rare genetic disorder that affects the body's ability to break down glycogen. Symptoms can include muscle weakness, breathing problems, and heart problems.
5. Mucopolysaccharidoses (MPS): These are a group of genetic disorders that affect the body's ability to break down sugar molecules. Symptoms can include joint stiffness, developmental delays, and heart problems.
Inborn errors of carbohydrate metabolism can be diagnosed through blood tests, urine tests, and other diagnostic procedures. Treatment depends on the specific disorder and may involve a combination of dietary changes, medication, and other therapies.
Henipavirus infections can cause a range of symptoms, including fever, headache, muscle weakness, confusion, and respiratory problems such as coughing and shortness of breath. In severe cases, these infections can lead to encephalitis (inflammation of the brain), which can be fatal.
Henipavirus infections are diagnosed through laboratory tests, such as PCR (polymerase chain reaction) or ELISA (enzyme-linked immunosorbent assay). Treatment is typically supportive, with care focusing on relieving symptoms and managing complications. Antiviral medications may be used in some cases, but their effectiveness is limited.
Prevention of henipavirus infections primarily involves avoiding contact with infected animals or bats, and taking precautions such as wearing protective clothing and gloves when handling animals or bat specimens. Vaccines are also being developed to protect against henipavirus infections.
Overall, henipavirus infections are rare but potentially life-threatening diseases that require prompt medical attention and careful management to prevent complications and improve outcomes.
Pseudorabies is characterized by fever, anorexia, lethargy, and a characteristic skin rash on the face, neck, and limbs. In severe cases, the disease can cause inflammation of the central nervous system (CNS), respiratory distress, and death.
The pseudorabies virus is primarily transmitted through close contact with infected animals or their bodily fluids, such as saliva, urine, or feces. The virus can also be spread through contaminated objects, such as needles or surgical instruments, or through the bite of an infected animal.
Pseudorabies is typically diagnosed based on a combination of clinical signs, laboratory tests (such as PCR or ELISA), and serology. There is no specific treatment for the disease, but antiviral medications may be used in severe cases to reduce the severity of symptoms.
In humans, pseudorabies is a rare disease that is typically associated with exposure to infected animals or contaminated objects. The disease is more common in people who work with swine or other animals, such as veterinarians or farmers. In rare cases, pseudorabies has been transmitted through organ transplantation or blood transfusion.
Prevention of pseudorabies primarily involves avoiding contact with infected animals and taking precautions to prevent the spread of the virus. This includes wearing protective clothing and gloves when handling animals, properly disinfecting equipment and surfaces, and ensuring that all animal products are thoroughly cooked before consumption.
In summary, pseudorabies is a viral disease that affects swine and other animals, as well as humans in rare cases. It is caused by the pseudorabies virus and can be transmitted through close contact with infected animals or contaminated objects. While there is no specific treatment for the disease, antiviral medications may be used in severe cases to reduce the severity of symptoms. Prevention primarily involves avoiding contact with infected animals and taking precautions to prevent the spread of the virus.
Examples of experimental liver neoplasms include:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and can be induced experimentally by injecting carcinogens such as diethylnitrosamine (DEN) or dimethylbenz(a)anthracene (DMBA) into the liver tissue of animals.
2. Cholangiocarcinoma: This type of cancer originates in the bile ducts within the liver and can be induced experimentally by injecting chemical carcinogens such as DEN or DMBA into the bile ducts of animals.
3. Hepatoblastoma: This is a rare type of liver cancer that primarily affects children and can be induced experimentally by administering chemotherapy drugs to newborn mice or rats.
4. Metastatic tumors: These are tumors that originate in other parts of the body and spread to the liver through the bloodstream or lymphatic system. Experimental models of metastatic tumors can be studied by injecting cancer cells into the liver tissue of animals.
The study of experimental liver neoplasms is important for understanding the underlying mechanisms of liver cancer development and progression, as well as identifying potential therapeutic targets for the treatment of this disease. Animal models can be used to test the efficacy of new drugs or therapies before they are tested in humans, which can help to accelerate the development of new treatments for liver cancer.
Respirovirus infections are a group of viral infections that affect the respiratory system, including the nose, throat, and lungs. These infections are caused by members of the Paramyxoviridae family of viruses, which include the respiratory syncytial virus (RSV), human metapneumovirus (HMPV), and human parainfluenza virus (HPIV).
The symptoms of respirovirus infections can vary depending on the age of the individual and the severity of the infection. In infants and young children, the symptoms may include coughing, sneezing, runny nose, fever, and difficulty breathing. In older children and adults, the symptoms may be more mild and may include a stuffy nose, sore throat, and cough.
Respirovirus infections are usually spread through contact with an infected person's respiratory secretions, such as mucus and saliva. The viruses can also survive on surfaces for a period of time and be transmitted through touching contaminated surfaces and then touching the face.
There is no specific treatment for respirovirus infections, but antiviral medications may be prescribed in severe cases. Treatment is generally focused on relieving symptoms and managing complications, such as pneumonia or bronchiolitis. In some cases, hospitalization may be necessary to provide supportive care, such as oxygen therapy and mechanical ventilation.
Prevention of respirovirus infections is important, especially for high-risk individuals such as infants, young children, and people with weakened immune systems. Preventative measures include frequent handwashing, avoiding close contact with people who are sick, and practicing good hygiene. Vaccines are also available for some types of respirovirus infections, such as RSV, and can help protect against infection.
CDGs are caused by mutations in genes that code for enzymes involved in glycosylation, a process that adds sugars to proteins and lipids to form glycoproteins and glycolipids. These molecules play important roles in cell signaling, protein folding, and the immune response. Without proper glycosylation, these molecules cannot function properly, leading to a wide range of symptoms and complications.
Symptoms of CDGs can vary depending on the specific disorder and the organs affected. Common symptoms include developmental delays, intellectual disability, seizures, poor muscle tone, and liver problems. Some children with CDGs may also experience failure to thrive, diarrhea, and vomiting.
There is currently no cure for CDGs, but various treatments are available to manage the symptoms and prevent complications. These may include enzyme replacement therapy, nutritional supplements, and medications to control seizures and other symptoms. In some cases, a bone marrow transplant may be necessary to replace the defective cells with healthy ones.
The diagnosis of CDG is based on a combination of clinical symptoms, laboratory tests, and genetic analysis. Newborn screening is increasingly being used to identify CDGs in infants, allowing for early intervention and treatment.
Overall, congenital disorders of glycosylation are rare and complex conditions that require specialized care and management. With advances in medical technology and research, there is hope for improved treatments and outcomes for individuals with CDGs.
Herpes simplex virus 1 (HSV-1) typically causes cold sores or fever blisters that appear on the lips, mouth, or nose. While herpes simplex virus 2 (HSV-2) is responsible for genital herpes which affects the genital area, buttocks, and anal area.
The infection can be spread through direct contact with an infected person's saliva, mucus, or skin, even if there are no visible sores present. Symptoms of herpes simplex may include itching, burning, tingling, redness, and small blisters that burst and ooze fluid.
There is no cure for herpes simplex, but medications can help manage symptoms and shorten the duration of an outbreak. Antiviral drugs such as acyclovir, famciclovir, and valacyclovir are commonly used to treat herpes simplex.
Types of Ovarian Cysts:
1. Functional cysts: These cysts form during the menstrual cycle and are usually small and disappear on their own within a few days or weeks.
2. Follicular cysts: These cysts form when a follicle (a tiny sac containing an egg) does not release an egg and instead fills with fluid.
3. Corpus luteum cysts: These cysts form when the corpus luteum (the sac that holds an egg after it's released from the ovary) does not dissolve after pregnancy or does not produce hormones properly.
4. Endometrioid cysts: These cysts are formed when endometrial tissue (tissue that lines the uterus) grows outside of the uterus and forms a cyst.
5. Cystadenomas: These cysts are benign tumors that grow on the surface of an ovary or inside an ovary. They can be filled with a clear liquid or a thick, sticky substance.
6. Dermoid cysts: These cysts are formed when cells from the skin or other organs grow inside an ovary. They can contain hair follicles, sweat glands, and other tissues.
Symptoms of Ovarian Cysts:
1. Pelvic pain or cramping
2. Bloating or discomfort in the abdomen
3. Heavy or irregular menstrual bleeding
4. Pain during sex
5. Frequent urination or difficulty emptying the bladder
6. Abnormal vaginal bleeding or spotting
Diagnosis and Treatment of Ovarian Cysts:
1. Pelvic examination: A doctor will check for any abnormalities in the reproductive organs.
2. Ultrasound: An ultrasound can help identify the presence of a cyst and determine its size, location, and composition.
3. Blood tests: Blood tests can be used to check hormone levels and rule out other conditions that may cause similar symptoms.
4. Laparoscopy: A laparoscope (a thin tube with a camera and light) is inserted through a small incision in the abdomen to visualize the ovaries and remove any cysts.
5. Surgical removal of cysts: Cysts can be removed by surgery, either through laparoscopy or open surgery.
6. Medications: Hormonal medications may be prescribed to shrink the cyst and alleviate symptoms.
It is important to note that not all ovarian cysts cause symptoms, and some may go away on their own without treatment. However, if you experience any of the symptoms mentioned above or have concerns about an ovarian cyst, it is essential to consult a healthcare provider for proper diagnosis and treatment.
Myelin oligodendrocyte glycoprotein
Herpesvirus glycoprotein B
Envelope glycoprotein GP120
Variant surface glycoprotein
Platelet membrane glycoprotein
Lysosome-associated membrane glycoprotein
Nuclear pore glycoprotein p62
Tumor-associated glycoprotein 72
Glycoprotein hormones, alpha polypeptide
Lipid-binding serum glycoprotein
Structure and function of respiratory syncytial virus surface glycoproteins - PubMed
DailyMed - Search Results for P-Glycoprotein Inhibitors
Glycoprotein VI deficiency: MedlinePlus Genetics
Labelling of membrane glycoproteins of cultivated Plasmodium falciparum*
NIH VideoCast - Structural Studies of Coronavirus Fusion Glycoproteins
Gp1ba glycoprotein 1b, alpha polypeptide [Mus musculus (house mouse)] - Gene - NCBI
Inhibition of platelet aggregation by native and desialised alpha-1 acid glycoprotein | Nature
A novel FKRP mutation in congenital muscular dystrophy disrupts the dystrophin glycoprotein complex
Chain A, Spike glycoprotein - Protein - NCBI
Glycoprotein IIb/IIIa induced coronary thrombolysis | Heart
Bioinformatics analysis and characteristics of envelop glycoprotein E epitopes of dengue virus
WikiGenes - Mog - myelin oligodendrocyte glycoprotein
Fusion glycoprotein F0 (Newcastle disease virus (STRAIN TEXAS)) | Protein Target - PubChem
JCI - Citations to Platelet glycoproteins Ia, Ic, and IIa are physicochemically indistinguishable from the very late activation...
positive regulation of glycoprotein biosynthetic process Antibodies | Invitrogen ...
The neuroprotective effect of brain -derived neurotrophic factor against human immunodeficiency virus type-1 glycoprotein 120...
DFG funds HITS research on SARS CoV-2 spike glycoprotein - HITS
P-Glycoprotein Removes Alzheimer's-Associated Toxin From the Brain - Neuroscience News
The "lecithotrophic" sea urchin Heliocidaris erythrogramma lacks typical yolk platelets and yolk glycoproteins. | Scholars@Duke
Human GP5 (Glycoprotein V, Platelet) CLIA Kit | G-EC-01063 | Gentaur Clia Kits
Human T-cell surface glycoprotein CD3 epsilon chain ELISA Kit
Characterization of disease-associated N-linked glycoproteins.
In vitro mucus glycoprotein production by colonic tissue from patients with ulcerative colitis. | Gut
Binding of bupivacaine to human serum proteins, isolated albumin and isolated alpha-1-acid glycoprotein. Differences between...
Role of a lipid intermediate in the transfer of mannose to endogenous glycoprotein acceptors in Aspergillus niger
Structural Characterization of HIV Env Glycoprotein by LC-MS | NIH Research Festival
THE ONTOGENY OF P-GLYCOPROTEIN IN THE DEVELOPING HUMAN BLOOD BRAIN BARRIER: IMPLICATION FOR OPIOID TOXICITY IN NEONATES |...
RePub, Erasmus University Repository: Use of platelet glycoprotein IIb/IIIa inhibitors in diabetics undergoing PCI for non-ST...
- The major envelope glycoprotein E of dengue (DEN) virus plays a central role in the biology of flaviviruses. (scirp.org)
Alpha-1 acid glyco2
- Coronavirus spike (S) glycoprotein trimers promote the virus's entry into cells and are the main targets of the humoral immune response. (nih.gov)
- Rebecca Wade and the Molecular and Cellular Modeling group at HITS use computational methods and simulations to investigate the mechanisms by which heparin and heparan sulfate proteoglycans interact with SARS-CoV-2 spike glycoprotein, and thereby affect host cell infection and host susceptibility. (h-its.org)
- SARS-CoV-2 Spike glycoprotein, Californian Variant B.1.429. (biovendor.com)
- Graphic representation of the interaction between the MERS-CoV spike glycoprotein (blue-purple) and its receptor dipeptidyl peptidase 4 (DPP4). (nih.gov)
- Platelet glycoprotein VI-related clinical defects. (medlineplus.gov)
- Defective Association of the Platelet Glycoprotein Ib-IX Complex with the Glycosphingolipid-Enriched Membrane Domain Inhibits Murine Thrombus and Atheroma Formation. (nih.gov)
- Critical role of platelet glycoprotein ibα in arterial remodeling. (nih.gov)
- Genetic deletion of platelet glycoprotein Ib alpha but not its extracellular domain protects from atherosclerosis. (nih.gov)
- In order to spare the young patient with severe symptoms an aortocoronary bypass operation, we decided to administer the glycoprotein IIb/IIIa receptor blocker tirofiban. (bmj.com)
- Aggressive antiplatelet treatment with tirofiban, a potent inhibitor of glycoprotein IIb/IIIa receptors on the surface of platelets, in combination with low molecular weight heparin, led to complete thrombolysis in the affected coronary vessels of this patient with unstable angina. (bmj.com)
- Background: The most recent ESC guidelines for percutaneous coronary intervention (PCI) recommend the use of glycoprotein IIb/IIIa inhibitors (GPI) in high risk patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS), particularly in diabetics. (eur.nl)
- These glycoproteins serve as machinery that enables them to reach out and grab onto the surrounding endosome membrane, which ultimately will be fused with the virus's own membrane. (nih.gov)
- Evaluation of protection in grazing lambs immunised with different doses of Haemonchus contortus gut membrane glycoproteins in Southern Brazil. (bvsalud.org)
- Platelets play a primary role in this process, interacting with subendothelium-bound von Willebrand factor (vWf) via the membrane glycoprotein (GP) Ib complex. (medscape.com)
- Citations to Platelet glycoproteins Ia, Ic, and IIa are physicochemically indistinguishable from the very late activation antigens adhesion-related proteins of lymphocytes and other cell types. (jci.org)
- Platelet glycoproteins Ia, Ic, and IIa are physicochemically indistinguishable from the very late activation antigens adhesion-related proteins of lymphocytes and other cell types. (jci.org)
- The very late activation antigens (VLA) are a subset of the superfamily of cell surface glycoproteins that serve as receptors from extracellular matrix proteins. (jci.org)
- Using a polyclonal antibody prepared against yolk glycoproteins from the typical developer Stronglyocentrotus purpuratus, we found that H. tuberculata contains cross-reactive proteins in abundance, but H. erythrogramma does not. (duke.edu)
- In the opening seconds, you see how receptor binding glycoproteins (light blue), which are proteins with a carbohydrate attached on the viral surface, dock with protein receptors (yellow) on a host cell. (nih.gov)
- Henipaviruses possess two envelope glycoproteins , the attachment (G) and the fusion (F) proteins that mediate cellular entry and are the major targets of virus - neutralizing antibody responses. (bvsalud.org)
- Cluster of Differentiation-200 (CD200) is an anti-inflammatory glycoprotein expressed in neurons, T cells, and B cells, and its receptor is expressed on glia. (nih.gov)
- The F protein is the major target for antiviral drug development, and both G and F glycoproteins are the antigens targeted by neutralizing antibodies induced by infection. (nih.gov)
- Glycoprotein VI deficiency can be caused by mutations in the GP6 gene, which provides instructions for making a protein called glycoprotein VI (GPVI). (medlineplus.gov)
- As a result, there is a shortage (deficiency) of functional GPVI protein on the surface of platelets, which leads to bleeding problems characteristic of glycoprotein VI deficiency. (medlineplus.gov)
- In Vitro-In Vivo Extrapolation Scaling Factors for Intestinal P-glycoprotein and Breast Cancer Resistance Protein: Part II. (aspetjournals.org)
- Literature-collated REFs ranged from 0.4 to 5.1 and 1.1 to 90 for intestinal P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP), respectively. (aspetjournals.org)
- Beta 2-glycoprotein-1 (apolipoprotein H) excretion in chronic renal tubular disorders: comparison with other protein markers of tubular malfunction. (bmj.com)
- Investigators at the Vaccine Research Center (VRC) of the National Institute of Allergy and Infectious Diseases (NIAID) have generated an hMPV fusion glycoprotein ("F protein") stabilized in a prefusion conformation. (nih.gov)
- Without GPVI binding to collagen, platelets cannot come together efficiently to form a clot, leading to the bleeding problems associated with glycoprotein VI deficiency. (medlineplus.gov)
- The "lecithotrophic" sea urchin Heliocidaris erythrogramma lacks typical yolk platelets and yolk glycoproteins. (duke.edu)
- Structural studies of coronavirus fusion glycoproteins / David Veesler, Ph.D., University of Washington. (nih.gov)
- Characterization of disease-associated N-linked glycoproteins. (nih.gov)
- In this review, we summarize common strategies for N-linked glycoprotein characterization and applications of these strategies to identification of glycoprotein changes associated with disease states. (nih.gov)
- Here we demonstrated the strategy to meet these challenges, and to highlight some inevitable problems with this glycoprotein characterization in the analytical field. (nih.gov)
- However, it is still un-clear where the well-defined B-cell epitopes for glycoprotein E which induce the neutralizing an-tibodies locates. (scirp.org)
- If you could find a way to induce more P-glycoprotein in the protective blood-brain barrier for people who are susceptible to Alzheimer's disease, perhaps they could take such a treatment and it would help postpone or prevent the onset of the disease," he said. (neurosciencenews.com)
- A paper on extraction, curation and comparison of literature data for a key transporter in drug discovery P-glycoprotein Uniprot:P08183 (aka MDR1, pgp, etc ). (blogspot.com)
- The two major glycoproteins on the surface of the respiratory syncytial virus (RSV) virion, the attachment glycoprotein (G) and the fusion glycoprotein (F), control the initial phases of infection. (nih.gov)
- As more of those fusion glycoproteins grab on, fold back on themselves, and form into hairpin-like shapes, they pull the membranes together. (nih.gov)
- In addition to Hendra virus and Nipah virus tetrameric sG and trimeric sF production , we also describe the expression and purification of Cedar virus tetrameric sG and Ghana virus trimeric sF glycoproteins . (bvsalud.org)
- These henipavirus glycoproteins were also used as immunizing antigens to generate monoclonal antibodies , and binding was demonstrated with a pan- henipavirus multiplex microsphere immunoassay . (bvsalud.org)
- In vitro mucus glycoprotein production by colonic tissue from patients with ulcerative colitis. (bmj.com)
- Hermans C, Wittevrongel C, Thys C, Smethurst PA, Van Geet C, Freson K. A compound heterozygous mutation in glycoprotein VI in a patient with a bleeding disorder. (medlineplus.gov)
- We have identified them as previously characterized platelet surface glycoproteins and have compared them with VLA molecules isolated from lymphocytes and other cells. (jci.org)
- Amyloid-β is maybe five times bigger than the small, drug-like molecules that P-glycoproteins are well-known to move. (neurosciencenews.com)
- Although assays for these glycoproteins have potential clinical utility, research is needed to translate these glycoproteins to clinical biomarkers. (nih.gov)
- The strategies of the vaccine-development programs have been focused on the HIV Env surface glycoprotein (Env), which enables the virus to enter host cells. (nih.gov)
- In this chapter, we review the structure and function of the RSV surface glycoproteins, including recent X-ray crystallographic data of the F glycoprotein in its pre- and postfusion conformations, and discuss how this information informs antigen selection and vaccine development. (nih.gov)
- Once inside the endosome, the acidic environment makes other glycoproteins (red, blue, yellow) on the viral surface change shape and become more flexible and dynamic. (nih.gov)
- We also review the N-linked glycoproteins altered in diseases such as breast cancer, lung cancer, and prostate cancer. (nih.gov)
- Thus, in order to characterize the role of glycoprotein E in the pathogenesis of dengue virus infection, we first used network servers (http://bio.dfci. (scirp.org)
- Glycoprotein VI deficiency is a bleeding disorder associated with a decreased ability to form blood clots. (medlineplus.gov)
- Orthologous to human GP1BA (glycoprotein Ib platelet subunit alpha). (nih.gov)
- T Annotating Human P-Glycoprotein Bioassay Data %J Mol. (blogspot.com)
- Drew WL, Chou S, Miner RC, Mohr BA, Busch MP, van der Horst CM, Asmuth DM, Kalish LA. Cytomegalovirus glycoprotein B groups in human immunodeficiency virus-infected patients with incident retinitis. (nih.gov)
- A team of SMU biological scientists has confirmed that P-glycoprotein (P-gp) has the ability to remove a toxin from the brain that is associated with Alzheimer's disease. (neurosciencenews.com)
- N-linked glycoproteins play important roles in biological processes, including cell-to-cell recognition, growth, differentiation, and programmed cell death. (nih.gov)
- P-glycoprotein, a critical toxin pump in the body, has the ability to remove amyloid plaques from the brain. (neurosciencenews.com)
- These acquired cases of glycoprotein VI deficiency are associated with autoimmune disorders such as immune thrombocytopenia purpura, Graves' disease , or systemic lupus erythematosus (SLE). (medlineplus.gov)
- Specific N-linked glycoprotein changes are associated with disease progression and identification of these N-linked glycoproteins has potential for use in disease diagnosis, prognosis, and prediction of treatments. (nih.gov)
- Because people with glycoprotein VI deficiency cannot form blood clots normally, they have an increased risk of nosebleeds (epistaxis) and may experience abnormally heavy or prolonged bleeding following minor injury or surgery. (medlineplus.gov)
- The platelet glycoproteins GPIIa and GPIc form a second mixed heterodimer. (jci.org)
- 2003) A ligand-binding pockets in the dengue virus envelop glycoprotein. (scirp.org)
- Winzler, R. in Glycoproteins of Blood Cells and Plasma (eds Jamieson, G. A. & Greenwald, T. J.) 204-218 (Lippincott, New York, 1971). (nature.com)