Click Chemistry: Organic chemistry methodology that mimics the modular nature of various biosynthetic processes. It uses highly reliable and selective reactions designed to "click" i.e., rapidly join small modular units together in high yield, without offensive byproducts. In combination with COMBINATORIAL CHEMISTRY TECHNIQUES, it is used for the synthesis of new compounds and combinatorial libraries.Neurosciences: The scientific disciplines concerned with the embryology, anatomy, physiology, biochemistry, pharmacology, etc., of the nervous system.Fagopyrum: A plant genus of the family POLYGONACEAE that is used as an EDIBLE GRAIN. Although the seeds are used as cereal, the plant is not one of the cereal grasses (POACEAE).Medical Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency.Satiety Response: Behavioral response associated with the achieving of gratification.Glucose Metabolism Disorders: Pathological conditions in which the BLOOD GLUCOSE cannot be maintained within the normal range, such as in HYPOGLYCEMIA and HYPERGLYCEMIA. Etiology of these disorders varies. Plasma glucose concentration is critical to survival for it is the predominant fuel for the CENTRAL NERVOUS SYSTEM.Food: Any substances taken in by the body that provide nourishment.Day Care: Institutional health care of patients during the day. The patients return home at night.Alkynes: Hydrocarbons with at least one triple bond in the linear portion, of the general formula Cn-H2n-2.Food, Formulated: Food and dietary formulations including elemental (chemically defined formula) diets, synthetic and semisynthetic diets, space diets, weight-reduction formulas, tube-feeding diets, complete liquid diets, and supplemental liquid and solid diets.Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Musculoskeletal System: The MUSCLES, bones (BONE AND BONES), and CARTILAGE of the body.Calcification, Physiologic: Process by which organic tissue becomes hardened by the physiologic deposit of calcium salts.Forelimb: A front limb of a quadruped. (The Random House College Dictionary, 1980)Bone and Bones: A specialized CONNECTIVE TISSUE that is the main constituent of the SKELETON. The principle cellular component of bone is comprised of OSTEOBLASTS; OSTEOCYTES; and OSTEOCLASTS, while FIBRILLAR COLLAGENS and hydroxyapatite crystals form the BONE MATRIX.Cumulative Trauma Disorders: Harmful and painful condition caused by overuse or overexertion of some part of the musculoskeletal system, often resulting from work-related physical activities. It is characterized by inflammation, pain, or dysfunction of the involved joints, bones, ligaments, and nerves.Bone Density: The amount of mineral per square centimeter of BONE. This is the definition used in clinical practice. Actual bone density would be expressed in grams per milliliter. It is most frequently measured by X-RAY ABSORPTIOMETRY or TOMOGRAPHY, X RAY COMPUTED. Bone density is an important predictor for OSTEOPOROSIS.Tendons: Fibrous bands or cords of CONNECTIVE TISSUE at the ends of SKELETAL MUSCLE FIBERS that serve to attach the MUSCLES to bones and other structures.Musculoskeletal Diseases: Diseases of the muscles and their associated ligaments and other connective tissue and of the bones and cartilage viewed collectively.Bone Development: The growth and development of bones from fetus to adult. It includes two principal mechanisms of bone growth: growth in length of long bones at the epiphyseal cartilages and growth in thickness by depositing new bone (OSTEOGENESIS) with the actions of OSTEOBLASTS and OSTEOCLASTS.

Resistance of paroxysmal nocturnal hemoglobinuria cells to the glycosylphosphatidylinositol-binding toxin aerolysin. (1/479)

Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal stem cell disorder caused by a somatic mutation of the PIGA gene. The product of this gene is required for the biosynthesis of glycosylphosphatidylinositol (GPI) anchors; therefore, the phenotypic hallmark of PNH cells is an absence or marked deficiency of all GPI-anchored proteins. Aerolysin is a toxin secreted by the bacterial pathogen Aeromonas hydrophila and is capable of killing target cells by forming channels in their membranes after binding to GPI-anchored receptors. We found that PNH blood cells (erythrocytes, lymphocytes, and granulocytes), but not blood cells from normals or other hematologic disorders, are resistant to the cytotoxic effects of aerolysin. The percentage of lysis of PNH cells after aerolysin exposure paralleled the percentage of CD59(+) cells in the samples measured by flow cytometry. The kinetics of red blood cell lysis correlated with the type of PNH erythrocytes. PNH type III cells were completely resistant to aerolysin, whereas PNH type II cells displayed intermediate sensitivity. Importantly, the use of aerolysin allowed us to detect PNH populations that could not be detected by standard flow cytometry. Resistance of PNH cells to aerolysin allows for a simple, inexpensive assay for PNH that is sensitive and specific. Aerolysin should also be useful in studying PNH biology.  (+info)

Identification of the individual residues that determine human CD59 species selective activity. (2/479)

Formation of the cytolytic membrane attack complex of complement on host cells is inhibited by the membrane-bound glycoprotein, CD59. The inhibitory activity of CD59 is species restricted, and human CD59 is not effective against rat complement. Previous functional analysis of chimeric human/rat CD59 proteins indicated that the residues responsible for the species selective function of human CD59 map to a region contained between positions 40 and 66 in the primary structure. By comparative analysis of rat and human CD59 models and by mutational analysis of candidate residues, we now identify the individual residues within the 40-66 region that confer species selective function on human CD59. All nonconserved residues within the 40-66 sequence were substituted from human to rat residues in a series of chimeric human/rat CD59 mutant proteins. Functional analysis revealed that the individual human to rat residue substitutions F47A, T51L, R55E, and K65Q each produced a mutant human CD59 protein with enhanced rat complement inhibitory activity with the single F47A substitution having the most significant effect. Interestingly, the side chains of the residues at positions 47, 51, and 55 are all located on the short single helix (residues 47-55) of CD59 and form an exposed continuous strip parallel to the helix axis. A single human CD59 mutant protein containing rat residue substitutions at all three helix residues produced a protein with species selective activity comparable to that of rat CD59. We further found that synthetic peptides spanning the human CD59 helix sequence were able to inhibit the binding of human CD59 to human C8, but had little effect on the binding of rat CD59 to rat C8.  (+info)

Complement activation and expression of membrane regulators in the middle ear mucosa in otitis media with effusion. (3/479)

The aetiopathogenesis of chronic otitis media with effusion (OME) in children is not yet fully understood. OME is characterized by metaplasia of the epithelium and accumulation of sticky, glue-like effusion in the middle ear containing different mediators of inflammation, including activation fragments of the complement system. Here we examined whether the fluid phase complement activation is reflected in the middle ear mucosa and how the mucosa is protected against the cytolytic activity of complement. Mucosal biopsies from 18 middle ears of children with a history of chronic OME were taken. The biopsies were analysed by immunofluorescence microscopy after staining for complement fragments iC3b/C3c, C3d and C9, and regulators membrane cofactor protein (MCP; CD46), decay-accelerating factor (DAF; CD55) and protectin (CD59). There was a strong staining for iC3b/C3c, and a weaker one for C3d and C9 on the surface of the middle ear epithelial cells of OME patients but not in controls without OME. MCP was expressed on the hyperplastic three to four outer cell layers of the epithelium, while CD59 was expressed throughout the middle ear mucosa. The results suggest a strong ongoing complement activation and consequent inflammation in the middle ear cavity. Unrestricted complement damage of the epithelial lining is prevented by the strong expression of MCP and CD59.  (+info)

Induction of decay-accelerating factor by cytokines or the membrane-attack complex protects vascular endothelial cells against complement deposition. (4/479)

Vascular endothelium is continuously exposed to complement-mediated challenge, and this is enhanced during inflammation. Although the complement-regulatory proteins decay-accelerating factor (DAF), CD59, and membrane cofactor protein (MCP) protect endothelial cells (ECs) against complement-mediated injury, the control of their expression and relative contributions to vascular protection is unclear. We explored the hypothesis that mechanisms exist which induce upregulation of complement-regulatory proteins on ECs to maintain vascular function in inflammation. Tumor necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma) each increased DAF expression but not CD59 or MCP expression, and a combination of these cytokines was more potent than either alone. Cytokine-induced expression depended on increased DAF mRNA and de novo protein synthesis and was maximal by 72 hours. In addition, assembly of the membrane-attack complex (MAC) on ECs induced a 3-fold increase in DAF expression, and this was enhanced by cytokines. DAF upregulation was not inhibited by protein kinase C (PKC) antagonists. The increase in DAF was functionally relevant since it reduced complement 3 (C3) deposition by 40%, and this was inhibited by an anti-DAF monoclonal antibody. These observations indicate that upregulation of DAF expression by cytokines or MAC may represent an important feedback mechanism to maintain the integrity of the microvasculature during subacute and chronic inflammatory processes involving complement activation.  (+info)

Synovial PMN show a coordinated up-regulation of CD66 molecules. (5/479)

Changes in the expression of various activation-dependent surface markers have been reported for polymorphonuclear neutrophils (PMN) isolated from synovial fluid of patients with inflammatory joint diseases. We extend these findings to the expression of CD66 molecules and several other surface markers. Three members of the CD66 family, namely CD66a, CD66b, and CD66c, showed an up to fourfold up-regulation on synovial fluid PMN compared with peripheral blood PMN (PBG) of the same patients; CD59 was increased twofold, the expression of CD16 did not change, whereas CD62L was reduced by more than 50% on synovial fluid PMN. It is interesting that CD66a, CD66b, and CD66c showed a coordinated expression on PBG of patients and controls and a coordinated up-regulation on synovial neutrophils. In contrast, after in vitro stimulation of peripheral blood PMN with phorbol myristate acetate, CD66c was much less up-regulated compared with CD66a and CD66b. All samples of synovial fluid PMN exhibited an additional increase in the expression of CD66a, CD66b, and CD66c when stimulated with phorbol myristate acetate in vitro. Prostaglandins are known to inhibit various responses of neutrophils to inflammatory stimuli. We could show that prostaglandins inhibit N-formyl-methionyl-leucyl-phenylalanine-induced up-regulation of CD66 on peripheral blood PMN in a concentration-dependent manner.  (+info)

Biochemical background of paroxysmal nocturnal hemoglobinuria. (6/479)

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired disorder characterized by paroxysms of intravascular hemolysis. A considerable part of erythrocytes in patient blood is susceptible to autologous complement activation because of the deficiency of CD59, which is a glycosylphosphatidylinositol (GPI)-anchored protein and inhibits the formation of the membrane attack complex (MAC) of complement. The deficiency of CD59 is derived from the inability of GPI-anchor synthesis. Although more than 10 proteins are involved in the GPI-anchor synthesis, the mutation of only one protein, PIG-A, causes the defect in about 200 patients with PNH who have been analyzed. The reason why only PIG-A causes the deficiency of GPI anchor is due to the location of its gene on X chromosome. The clonal stem cell mutated with PIG-A gene in the bone marrow loses the capability of the synthesis of GPI-anchor. The mutation of PIG-A gene alone, however, seems to be insufficient to account for the survival of the PIG-A-deficient cells in the bone marrow. Thus, a fraction of the mutant stem cells probably gain a survival advantage by some additional changes, either additional mutations or changes in immunological circumstances. The release of the surviving cells into blood stream results in a clinical syndrome with PNH.  (+info)

Development of adenovirus vectors encoding rat complement regulators for use in therapy in rodent models of inflammatory diseases. (7/479)

C activation has been implicated in the pathogenesis of numerous inflammatory human diseases and disease models. A therapy based on C inhibition might therefore be of benefit to reduce inflammation and ameliorate disease. C inhibition in vivo can be accomplished by the delivery of soluble recombinant C regulators either systemically or directly to a target site, but effects are transitory. We have developed a strategy for the efficient delivery of the membrane-bound rat C inhibitors, CD59, Crry, and decay-accelerating factor (DAF), using replication-deficient adenovirus vectors with the intention of treating rat models of disease in which C is implicated. The adenovirus recombinants(RAd), RAdCD59, RAdCrry, and RAdDAF, respectively, have been tested for expression and function of the transgene in vitro. Infection of human fetal foreskin fibroblasts resulted in high levels of expression of each of the rat inhibitors. The constructs were also tested for inhibition of rat C-mediated cell lysis and C3b deposition. In a cell lysis assay, each inhibited to varying degrees of efficiency in the order RAdCD59 = RAdDAF > RAdCrry. In a C3b deposition assay, RAdDAF caused a greater reduction in C3b deposition than RAdCrry and RAdCD59 was ineffective. These agents, individually or in combination, provide the tools for testing the effects of prolonged inhibition of C at a target site on the progress of experimental models of disease.  (+info)

Thyrotropin-releasing hormone-induced depletion of G(q)alpha/G(11)alpha proteins from detergent-insensitive membrane domains. (8/479)

The role of detergent-insensitive membrane domains (DIMs) in desensitisation of the G protein-coupled receptor-mediated hormone response was studied in clone E2M11 of HEK293 cells which stably express high levels of both thyrotropin-releasing hormone (TRH) receptors and G(11)alpha G protein. DIMs were prepared by flotation in equilibrium sucrose density gradients and characterised by a panel of membrane markers representing peripheral, glycosylphosphatidylinositol-bound as well as integral membrane proteins (caveolin, CD29, CD55, CD59, CD147, the alpha subunit of Na, K-ATPase) and enzyme activities (alkaline phosphatase, adenylyl cyclase). Caveolin-containing DIMs represented only a small fraction of the overall pool of G(q)alpha/G(11)alpha-rich domains. Prolonged stimulation of E2M11 cells with TRH resulted in dramatic depletion of G(q)alpha/G(11)alpha from all DIMs, which was paralleled by a concomitant G(q)alpha/G(11)alpha increase in the high-density gradient fractions containing the bulk-phase membrane constituents soluble in 1% Triton X-100. Distribution of membrane markers was unchanged under these conditions. Membrane domains thus represent a substantial structural determinant of the G protein pool relevant to desensitisation of hormone action.  (+info)

*CD59 antigen

... (also called 1F-5Ag, H19, HRF20, MACIF, MIRL, P-18 or protectin) inhibits formation of membrane attack complex ( ... CD molecules are leucocyte antigens on cell surfaces. CD antigens nomenclature is updated at Protein Reviews On The Web (http ... IPR003631 Cell-surface glycoprotein Ly-6/CD59 InterPro: IPR003632 ARS[disambiguation needed]; CD177; CD59; LY6D; LY6E; LY6H; ... Genetic defects in GPI-anchor attachment that cause a reduction or loss of both CD59 and CD55 on erythrocytes produce the ...

*Three-finger protein

Other LU proteins, such as the CD59 antigen, have well-studied functions in regulation of the immune system. Snake three-finger ... Other LU domain proteins are small globular proteins such as CD59 antigen, LYNX1, SLURP1, and SLURP2. Many LU domain containing ... The family is named for two representative groups of members, the small globular protein lymphocyte antigen 6 (LY6) family and ... "High-resolution structures of bacterially expressed soluble human CD59". Acta Crystallographica. Section F, Structural Biology ...

*CD59

... Antigen at the US National Library of Medicine Medical Subject Headings (MeSH) Human CD59 genome location and CD59 gene ... 1990). "The CD59 antigen is a structural homologue of murine Ly-6 antigens but lacks interferon inducibility". Eur. J. Immunol ... 1990). "Isolation and expression of the full-length cDNA encoding CD59 antigen of human lymphocytes". DNA Cell Biol. 9 (3): 213 ... 1992). "Structure of the CD59-encoding gene: further evidence of a relationship to murine lymphocyte antigen Ly-6 protein". ...

*List of MeSH codes (D23)

... antigens, cd57 MeSH D23.050.301.264.035.158 --- antigens, cd58 MeSH D23.050.301.264.035.159 --- antigens, cd59 MeSH D23.050. ... antigens, cd57 MeSH D23.101.100.110.158 --- antigens, cd58 MeSH D23.101.100.110.159 --- antigens, cd59 MeSH D23.101.100.110.179 ... hla-a antigens MeSH D23.050.301.500.450.370.372 --- hla-a1 antigen MeSH D23.050.301.500.450.370.374 --- hla-a2 antigen MeSH ... hla-b antigens MeSH D23.050.301.500.450.380.383 --- hla-b7 antigen MeSH D23.050.301.500.450.380.385 --- hla-b8 antigen MeSH ...

*CD2

... Antigen at the US National Library of Medicine Medical Subject Headings (MeSH) Mouse CD Antigen Chart Human CD Antigen ... "Overlapping but nonidentical binding sites on CD2 for CD58 and a second ligand CD59". Science. 256 (5065): 1805-7. doi:10.1126/ ... The great majority of T cell lymphomas and leukaemias also express CD2, making it possible to use the presence of the antigen ... It has also been called T-cell surface antigen T11/Leu-5, LFA-2, LFA-3 receptor, erythrocyte receptor and rosette receptor. It ...

*Schistosoma mansoni

Antibodies and antigens can be detected in the blood using ELISA to indentify infection. Adult worm antigens can be detected by ... In addition, schistosomes have six homologues of human CD59 which are strong inhibitors of MAC. The presence of S. mansoni is ... Circulating cathodic antigen (CCA) in urine can be tested with lateral flow immune-chromatographic reagent strip and point-of- ... This fibrosis occurs only many years after the infection and is presumed to be caused in part by soluble egg antigens and ...

*Extracellular RNA

Babiker, AA; Nilsson, B; Ronquist, G; Carlsson, L; Ekdahl, KN (February 1, 2005). "Transfer of functional prostasomal CD59 of ... "Tumor-derived exosomes are a source of shared tumor rejection antigens for CTL cross-priming". Nature Medicine. 7 (3): 297-303 ...

*Complement system

C3b binds to antigen-associated Ig and to the microbe surface. Ability of C3b to bind to antigen-associated Ig would work ... One example is CD59, also known as protectin, which inhibits C9 polymerisation during the formation of the membrane attack ... which has formed a complex with antigens. C4b and C3b are also able to bind to antigen-associated IgG or IgM, to its Fc portion ... Upon immunisation with an antigen, more of these receptors are formed, and they are then shed from the cells to circulate in ...

*CD9

... antigen is a protein that in humans is encoded by the CD9 gene. The protein encoded by this gene is a member of the ... Ninomiya H, Sims PJ (1992). "The human complement regulatory protein CD59 binds to the alpha-chain of C8 and to the "b"domain ... Boucheix C, Benoit P, Frachet P, Billard M, Worthington RE, Gagnon J, Uzan G (1991). "Molecular cloning of the CD9 antigen. A ... Higashihara M, Takahata K, Yatomi Y, Nakahara K, Kurokawa K (1990). "Purification and partial characterization of CD9 antigen ...

*Outline of immunology

Antigen Antigenicity Immunogen Superantigen Allergen Hapten Epitope Linear Conformational Mimotope Tumor antigen Antigen- ... CD59) - Classical, Lectin, Alternate Factor I - Classical, Lectin, Alternate C4BP - Classical, Lectin Factor H - Alternate ... T cells Antigen receptor - T cell receptor (TCR) Subunits - [email protected] / [email protected] / [email protected] / [email protected] Co-receptors CD8 (CD8α / CD8β) CD4 ... B cells Antigen receptor - B cell receptor (BCR) Subunits- Immunoglobulin heavy chain / Immunoglobulin light chain Co-receptors ...

*Xenotransplantation

Indirect xenorecognition involves the presentation of antigens from the xenograft by recipient antigen presenting cells to CD4+ ... Experiments have shown this reduces α-Gal expression by 70%. Expression of human complement regulators (CD55, CD46, and CD59) ... Antigens of phagocytosed graft cells can also be presented by the host's class I MHC molecules to CD8+ T cells. The strength of ... These antigens (foreign objects) are often treated with powerful immunosuppressive drugs that could, in turn, make the patient ...

*CD90

It was originally named theta (θ) antigen, then Thy-1 (THYmocyte differentiation antigen 1) due to its prior identification in ... it can also be involved in cell to cell transfer of GPI anchored proteins like CD55 and CD59. Thy-1 is one of the most heavily ... The antigen Thy-1 was the first T cell marker to be identified. Thy-1 was discovered by Reif and Allen in 1964 during a search ... "The AKR thymic antigen and its distribution in leukemias and nervous tissue". J. Exp. Med. 120: 413-433. doi:10.1084/jem.120.3. ...

*NCR3

2004). "CD59 is physically and functionally associated with natural cytotoxicity receptors and activates human NK cell-mediated ... Tissue Antigens. 58 (4): 255-8. doi:10.1034/j.1399-0039.2001.580406.x. PMID 11782277. "Entrez Gene: NCR3 natural cytotoxicity ...

*Primary immunodeficiency

This is carried out by using donor-derived antigen-presenting cells. These new methods have reduced culture time to 10-12 days ... CD59) deficiency Paroxysmal nocturnal hemoglobinuria Immunodeficiency associated with ficolin 3 deficiency These are a few ... recurrent infections and failure of the development of antibodies on exposure to antigens. The 1999 criteria also distinguish ... selective immunoglobulin A deficiency Specific antibody deficiency to specific antigens with normal B cell and normal Ig ...

*Complement control protein

DAF and CD59. This mechanism allows some tumours to evade complement action. Norman, D.G., Barlow, P.N., Baron, M., Day, A.J., ... and unwanted material such as cell debris and antibody-antigen complexes. Most of the complement control proteins act on the ...

*Decay-accelerating factor

List of human clusters of differentiation CD59 GRCh38: Ensembl release 89: ENSG00000196352 - Ensembl, May 2017 GRCm38: Ensembl ... Cromer blood group system at BGMUT Blood Group Antigen Gene Mutation Database at NCBI, NIH. ... red blood cells with very low levels of DAF and CD59 undergo complement-mediated hemolysis. DAF is used as a receptor by some ...

*Cholesterol-dependent cytolysin

... the recognition of CD59 membrane-anchored protein. The recognition of cholesterol provides specificity for eukaryotic cells and ... of the lectin regulatory domain of the cholesterol-dependent cytolysin lectinolysin reveals the basis for its lewis antigen ... the specificity for the glycosylphosphatidylinositol-anchored protein CD59 provides specificity for human cells. Even though ...
Definition of homologous restriction factor in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is homologous restriction factor? Meaning of homologous restriction factor as a legal term. What does homologous restriction factor mean in law?
Ebrahimi, K. B., Fijalkowski, N., Cano, M. and Handa, J. T. (2013), Decreased membrane complement regulators in the retinal pigmented epithelium contributes to age-related macular degeneration. J. Pathol., 229: 729-742. doi: 10.1002/path.4128 ...
RHEUMATOID ARTHRITIS. Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects mainly diarthrodial joints and periarticular structures, and can acquire a systemic character. Rheumatoid arthritis affects approximately 1% of the world population, being two to three times more common in women.1. The etiology of RA has not been completely clarified. However, environmental and genetic factors have contributed to the development of the disease. In the early stages of RA, proliferation and edema of the synovial layer cells occur, with infiltration of B and T cells, macrophages, and granulocytes. The synovium thickens, and the joint becomes swollen and painful. With progression, synovial proliferation leads to the formation of pannus, a tissue that invades the articular cartilage and bone. Joint destruction is irreversible. Osteoclasts reabsorb bone, and there is release of proteolytic enzymes, such as metal-loproteinases, aggrecanases, and cathepsins, responsible for the destruction of ...
Results Brain pathological injury was the most serious at 24 h after reperfusion, The complement regulatory protein CD46 expression decreased gradually after local cerebral ischaemia-reperfusion injury, the lowest at 24 h after reperfusion, and returned to normal at 96 h after reperfusion.complement regulatory protein CD46 expression was negative correlated with brain pathological injury.. ...
Background/Purpose: The influence of complement-mediated innate immune responses on cartilage and bone homeostasis in the ageing joint have not been studied. Inappropriate complement-mediated cell damage is prevented by membrane regulators such as CD59. Synovial tissue expression of CD59 is altered during inflammatory arthritis; elevated CD59 levels may be necessary to protect joint tissues. Roles of CD59 in maintaining tissue equilibrium and structural architecture within the synovial joint have not been described previously. Since CD59a is the primary regulator of membrane attack complex assembly in mice; we used CD59a-gene-deleted mice (CD59a-/-) as tools to unravel the function of CD59a in modulating age-related joint degeneration. Methods: Hind limbs were collected from C57BL/6J wild type (WT) and CD59a-/- mice at 8-, 20- and 50- weeks of age (6 to 10 mice/group). The Mankin score was used to classify the histopathological severity of osteoarthritic (OA) lesions. Three dimensional ...
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Simpson, R. J., Florida-James, G., Whyte, G. P., Middleton, N., Shave, R., George, K. & Guy, K. (2007). The effects of marathon running on expression of the complement regulatory proteins CD55 (DAF) and CD59 (MACIF) on red blood cells. European journal of applied physiology. 99, 201-204. doi:10.1007/s00421-006-0326-2. ISSN 1439-6327. ...
Simpson, R. J., Florida-James, G., Whyte, G. P., Middleton, N., Shave, R., George, K. & Guy, K. (2007). The effects of marathon running on expression of the complement regulatory proteins CD55 (DAF) and CD59 (MACIF) on red blood cells. European journal of applied physiology. 99, 201-204. doi:10.1007/s00421-006-0326-2. ISSN 1439-6327. ...
APT 3111 [APT 2392, CD59-Prodaptin™] is a derivative of the membrane-bound complement inhibitor CD59 and was under development with Adprotech (now Inflazyme
Objectives: To analyze the protective effects against complement-mediated cytolysis of the MCP, DAF, and CD59 human complement regulatory proteins, alone and in combination, on NIH 3T3 mouse fibroblast cells. Materials and Methods: We constructed 3 double and 3 single-human complement regulatory protein plasmids (pIRES-hMCP-hDAF, pIRES-hMCP-hCD59, pIRES-hDAF-hCD59, pIRES-A-hMCP, pIRES-B-hDAF, and pIRES-B-hCD59 ...
CRP seems to be not only a biomarker for atherosclerosis but also a mediator of plaque formation.3 By binding to enzymatically degraded low-density lipoprotein, CRP is able to activate the classical pathway of complement,13 serving as a potential link between complement activation and atherosclerosis.9,10 To protect against complement-mediated cell lysis, nucleated cells express complement inhibitor proteins on their surface. By upregulating the expression of these proteins in endothelial cells, CRP may serve to protect ECs from complement-mediated injury.. The ability of CRP to bind to nucleated cells and cause complement activation without cytolysis14 has been largely attributed to its ability to recruit the inhibitory plasma protein factor H.15 However, our results indicate that CRP may play a more active, protective role by stimulating the expression of DAF, CD46, and CD59 in endothelial cells. The kinetics of DAF expression were analyzed in greater detail because DAF seems to be the most ...
BACKGROUND: Pulmonary xenotransplantation is currently limited by hyperacute rejection mediated in part by xenoreactive natural antibody and complement. Transgenic swine organs that express the human complement regulatory protein CD59 have demonstrat
CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide, Mouse Monoclonal Antibody [Clone SPM616 ] validated in IHC, IF, FC (AH12772-100), Abgent
Scientists have discovered when a cancer-killing virus is injected in the bloodstream it hitches a ride on blood cells and evades attack from the immune sy
We have proposed that increased MAC deposition as a result of glycation inactivation of hCD59 could contribute to the pathogenesis of the vascular complications of human diabetes (8). Our current studies demonstrate that 1) glycated hCD59 is present and colocalizes with MAC in diabetic kidneys and endoneurial microvessels from diabetic but not from nondiabetic patients (Figs. 3 and 4, Table 2), 2) there is a significant reduction of hCD59 functional activity in diabetic RBCs demonstrated by an increased sensitivity to MAC-mediated lysis detected with two well-established methods of complement-mediated lysis (Fig. 5), and 3) there is significantly lower activity of hCD59 in RBCs from diabetic as compared with nondiabetic subjects (Fig. 5). Together, the results of this work indicate that glycation inactivates hCD59 in diabetic subjects and provide a probable molecular explanation for the reported findings of increased MAC deposition in diabetic kidneys (22), nerves (23), and retinas (24). These ...
The group of cells in the body that are affected by the genetic defect that causes PNH. These cells all come from the same parent cell in the bone marrow. Since the genetic defect lies in the parent cell, all cells which come from the parent cell, (including red blood cells, white blood cells and platelets) are affected. The size of a PNH clone depends on the number of cells affected by PNH. A PNH clone is tested on a regular basis in order to identify whether a PNH clone has increased, decreased or is stable. ...
CD59, 50 µg. CD59 (also known as HRF20, protectin) is a 20 kDa glycoprotein attached to the plasma membrane by a glycosylphosphatidylinositol (GPI) anchor.
Mohamed Kharfan-Dabaja, MD, discusses the future of PNH treatment, the various symptoms that can present in PNH, and the challenges that still remain for further improving outcomes.
Studies confirm the prognostic value of ENoG testing performed between 3 and 14 days after onset of complete facial paralysis. ...
TY - JOUR. T1 - Assessing donor chimerism using flow cytometry in paroxysmal nocturnal haemoglobinuria after stem cell transplantation--a case report.. AU - Raja Sabudin, Raja Zahratul Azma. AU - Hussin, Noor Hamidah. AU - Chooi Fun, Leong. AU - Ainoon, O.. AU - Cheong, S. K.. PY - 2006/12. Y1 - 2006/12. N2 - Paroxysmal nocturnal haemoglobinuria (PNH) is an acquired haemopoietic stem cell disorder arising from somatic mutation of the X-linked PIG-A gene which leads to deficiency of the glycosylphosphatidylinositol (GP1) membrane anchor proteins such as CD 59 (MIRL: membrane inhibitor of reactive lysis) and CD 55 (DAF: decay accelerating factor). Allogeneic peripheral blood stem cell transplant (PBSCT) is a curative mode of treatment in symptomatic PNH patients. Assessment of donor chimerism for PBSCT can be performed by various methods including short tandem repeat loci (STR) and variable number of tandem repeats (VNTR). Flow cytometry, which is much cheaper and faster, also can be used to ...
Treatment for paroxysmal nocturnal hemoglobinuria in HAL, Bangalore, find doctors near you. Book Appointment Online, View Fees, Reviews Doctors for Paroxysmal Nocturnal Hemoglobinuria Treatment in HAL, Bangalore | Practo
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Another name for Paroxysmal Nocturnal Hemoglobinuria is Paroxysmal Nocturnal Hemoglobinuria. What is paroxysmal nocturnal hemoglobinuria? A person with ...
Paroxysmal nocturnal hemoglobinuria: Find the most comprehensive real-world symptom and treatment data on paroxysmal nocturnal hemoglobinuria at PatientsLikeMe. 9 patients with paroxysmal nocturnal hemoglobinuria experience fatigue, depressed mood, pain, anxious mood, and insomnia.
Find the best paroxysmal nocturnal hemoglobinuria doctors in Thane. Get guidance from medical experts to select paroxysmal nocturnal hemoglobinuria specialist in Thane from trusted hospitals - credihealth.com
NEW HAVEN, Conn.--(BUSINESS WIRE)--Alexion Pharmaceuticals, Inc. (NASDAQ:ALXN) today announced the initiation of two Phase 3 trials of ALXN1210, a highly innovative, longer-acting anti-C5 antibody that inhibits terminal complement. The first trial is a Phase 3 open-label, multinational, active-controlled study of ALXN1210 compared to eculizumab (Soliris®) in complement inhibitor treatment-naïve patients with paroxysmal nocturnal hemoglobinuria (PNH).
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired disease characterized by clonal hematopoietic stem cell disorder, with increased mortality and morbidity. Venous thrombosis is the most common cause of mortality in PNH. The relationship between PNH and cerebrovascular disease is unclear; few cases are reported in the literature, most of them related to cerebral venous thrombosis; In PNH the involvement of intracranial and extracranial arterial sites is very rare. We report a case of a 49-year-old woman who has a medical history of diabetes mellitus, hypertension, and PNH and presented multiple lacunar strokes in a routine consultation with a hematologist ...
Paroxysmal nocturnal haemoglobinuria (PNH) is a unique disorder in which a substantial proportion of the patients red cells have an abnormal susceptibility to activated complement. This results from the presence of a clone that originates from a haematopoietic stem cell bearing an acquired somatic mutation in the X-linked gene ...
Learn about paroxysmal nocturnal hemoglobinuria. What are the symptoms, the causes and how to treat this condition? What can we do to cope...
Feldman L. Triiodothyronine (T3) toxicosis and paroxysmal nocturnal hemoglobinuria: report of case. J Am Osteopath Assoc 1981;80(7):491. doi: 10.7556/jaoa.1981.80.7.491.. Download citation file:. ...
Protectin D1 also known as neuroprotectin D1 (when it acts in the nervous system) and abbreviated most commonly as PD1 or NPD1 is a member of the class of specialized proresolving mediators. Like other members of this class of polyunsaturated fatty acid metabolites, it possesses strong anti-inflammatory, anti-apoptotic and neuroprotective activity. PD1 is an aliphatic acyclic alkene 22 carbons in length with two hydroxyl groups at the 10 and 17 carbon positions and one carboxylic acid group at the one carbon position. Specifically, PD1 is an endogenous stereoselective lipid mediator classified as an autocoid protectin. Autacoids are enzymatically derived chemical mediators with distinct biological activities and molecular structures. Protectins are signaling molecules that are produced enzymatically from unsaturated fatty acids. Their molecular structure is characterized by the presence of a conjugated system of double bonds. PD1, like other protectins, is produced by the oxygenation of the ω-3 ...
Severely anemic patients with PNH on treatment with Soliris™ can become transfusion-free with improved hemoglobin when switched to APL-2 monotherapy. Treatment-naïve patients with PNH show clinically meaningful improvements for all hematological parameters when treated with APL-2. CRESTWOOD, Ky. and WALTHAM, Mass., June 26, 2018 (GLOBE NEWSWIRE) -- Apellis Pharmaceuticals, Inc. (Nasdaq:APLS), a clinical-stage biopharmaceutical company focused on the development of novel therapeutic compounds to treat disease through the inhibition of the complement system, will provide clinical updates today on its two ongoing Phase Ib PNH studies during an R&D Day in New York between 2.00 pm and 5.00 pm.. Apellis is developing APL-2 for the treatment of PNH, a rare, acquired, potentially life-threatening disease characterized by complement-mediated thrombosis and hemolytic anemia. The Company believes that by targeting C3, APL-2 can improve hematological parameters in patients with PNH on treatment with C5 ...
陣發性夜間血紅素尿症(paroxysmal nocturnal haemoglobinuria, PNH)是一種罕見的造血幹細胞疾病,因後天基因突變而造成[1]。一般來說,正常紅血球的細胞膜上有幾種保護性蛋白質,例如:蛋白衰變加速因子(decay accelerating factor, CD55)以及溶解細胞膜抑制物(membrane inhibitor of reactive lysis, CD59),使紅血球不會因補體(免疫系統的一部分)的攻擊而破裂[1]。然而,PNH患者因為在X染色體上的phosphatidylinositol glycan A (PIG-A)基因發生突變,造成某些醣脂質,例如glycosylphosphatidylinositols (GPI)無法形成,而使紅血球上的保護性蛋白質無法藉著GPI結合在紅血球的細胞膜上[1]。紅血球沒有這些蛋白質的保護就容易因人體內補體系統的攻擊而破裂,引起持續、慢性的血管內溶血性疾病,這也是造成疾病症狀及後續嚴重併發症的原因[2-4 ...
Speaking with your healthcare team about your condition and finding out what you can about the disease can be empowering and can help you understand how best to move forward. OneSource is a complimentary, personalized patient support program offered by Alexion, and tailored to the specific needs of people living with aHUS, gMG, HPP, LAL-D, NMOSD and PNH. Were here to help you learn, and were here to help you understand the options available to you.. ...
This study was presented at the European Hematology Association annual meeting in June 2013. Abstract EHA18ABSSUB-4921 Petra Muus, H. Schrezenmeier, G. Socié, J. Maciejewski, J. Szer, R Brodsky, A. Urbano-Ispizua, M. Bessler, Y. Kanakura, W. Rosse, G. Khursigara, C. Bedrosian, P. Hillmen
Definition of Epidemic haemoglobinuria with photos and pictures, translations, sample usage, and additional links for more information.
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Soliris (eculizumab) is used to treat paroxysmal nocturnal hemoglobinuria. Includes Soliris side effects, interactions and indications.
Complement directly leads to the destruction of cells by causing a membrane attack complex to be formed and leading to apoptosis by creating a pore in the membrane. Antibodies can be used for tagging, but more often they just bind receptors so theyre useless or cause agglutination of invading particles etc ...
Complement directly leads to the destruction of cells by causing a membrane attack complex to be formed and leading to apoptosis by creating a pore in the membrane. Antibodies can be used for tagging, but more often they just bind receptors so theyre useless or cause agglutination of invading particles etc ...
Das C9-Gen kodiert die Complement Komponente 9. Diese ist am Membrane Attack Complex (MAC) beteiigt, welcher am Ende der Complementkaskade zur Auflösung der Zielbakterien führt. Mutationen können zu einem Mangel führen, wobei allerdings noch nicht klar ist, welchen Krankheitswert einem solchen Mangel zukommt.. ...
Das C8G-Gen kodiert die gamma Polypeptidkette des Complementfaktors 8. Dieser Faktor ist am membrane attack complex (MAC) beteiligt, welcher Poren in die Bakterienwände bestimmter Bakterien zu reißen und damit die Zerstörung herbeizuführen vermag. Erkrankungen sind bisher nicht mit Mutationen in diesem Gen in Zusammenhang gebracht worden.. ...
MI Update - Volume 12, Issue 4 is centered on immunology of the liver. Including articles of vein tolerance and development of regulator CD4 T-cells, IL-27R, and T-cell Immunity
A novel cell surface antigen has been identified on a wide range of lymphoid cells and erythrocytes. A mAb YTH 53.1 (CD59) against this antigen enhanced the lysis of human red cells and lymphocytes by homologous complement. Studies of reactive lysis using different species of C56, and of whole serum used as a source of C7-9, indicated that the inhibitory activity of the CD59 antigen is directed towards the homologous membrane attack complex. CD59 antigen was purified from human urine and erythrocyte stroma by affinity chromatography using the mAb YTH 53.1 immobilized on Sepharose, and, following transient expression of a human T cell cDNA library in COS cells, the corresponding cDNA also identified using the antibody. It was found that the CD59 antigen is a small protein (approximately 20 kD as judged by SDS-PAGE, 11.5 kD predicted from the isolated cDNA) sometimes associated with larger components (45 and 80 kD) in urine. The sequence of CD59 antigen is unlike that of other complement ...
This volume reviews the fundamental understanding of this potentially life-threatening disease and the advances in treatment that have been achieved with the use of the monoclonal antibody eculizumab. Although the PIGA gene has been known for many years, the mechanism of clonal dominance in paroxysmal nocturnal hemoglobinuria is still largely unknown. This book, Paroxysmal Nocturnal Hemoglobinuria, discusses the direction of continuing research in this area, as well as the potential for the development of management guidelines. It serves as a valuable source of information for both basic scientists and physicians, especially immunologists targeting GPI-anchored proteins and complements, and hematologists specializing in bone marrow failure. ...
SUMMARY In contrast to all other intrinsic abnormalities of the erythrocyte, paroxysmal nocturnal hemoglobinuria (PNH) is an acquired, not an inherited, disorder. PNH arises as a consequence of somatic mutation, involving one or more hematopoietic stem cells, of PIGA, a gene located on the X chromosome that is required for synthesis of the glycosylphosphatidylinositol (GPI) moiety that anchors some proteins to the cell surface. Consequently, all GPI-anchored proteins (GPI-APs) that are normally expressed are deficient on the mutant hematopoietic stem cells and their progeny. The complement-mediated intravascular hemolytic anemia and the resulting hemoglobinuria that are the clinical hallmarks of PNH are a consequence of deficiency of the GPI-anchored complement regulatory proteins, CD55 and CD59. Although PNH is a neoplastic (clonal) disease, it is not a malignant disease in that there is no exaggerated proliferation of neoplastic cells and replacement of marrow or spread to other tissues, and ...
Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal bone marrow disorder, resulting from an acquired, somatic X-linked mutation of the PIG-A gene in an hematopoietic stem cell. Absence of PIG-A function in a cell prevents synthesis of the glycosylphosphatidylinositol (GPI) moiety, which anchors many different types of proteins to the cell membrane. Intravascular red cell destruction, the hallmark of the disorder, is caused by susceptibility of the abnormal erythrocyte to complement-mediated lysis; this sensitivity is due to lack of CD59, a potent inhibitor of the late components of complement and reactive lysis. In vitro studies from this laboratory have demonstrated transfer of GPI-linked proteins, CD55 and CD59, from normal to deficient cells and transfer is associated with resistance to hemolysis. Patients with PNH frequently require transfusion as their standard care. In addition, patients with all blood groups requiring transfusion will often receive compatible group O blood. Group O ...
The kidney is particularly susceptible to complement-mediated injury in a number of clinical settings, and congenital deficiency or defects in the complement-regulatory proteins MCP and factor H are strongly associated with the development of renal disease. In the current study, we demonstrated that Crry (the murine homolog of MCP in the kidney) is the only membrane-bound regulator of complement expressed by murine TECs. Crry is expressed on the cell membrane, and its expression is concentrated in the basolateral portion of the cell. Polarized TECs regulate complement more efficiently on the basolateral surface of the cells than on the apical surface, in part because of Crry expression at this site. As with renal ischemia/reperfusion (I/R) (21), chemical hypoxia of the TECs causes a reduction in surface Crry levels, and the distribution within the cell is also altered.. Spontaneous complement activation on the surface of TECs is also controlled by endogenous factor H. When rH 19-20 was added to ...
Paroxysmal Nocturnal Haemoglobinuria (PNH) is an acquired hematopoietic stem-cell disorder related to the somatic mutation in PIG-A gene (X-chromosome). This genetic alteration results in partial or total deficiency of all proteins normally linked to the cell membrane by glycosylphosphatidyl-inositol (GPI). Flow cytometry provides an efficient diagnostic test in which the lack of GPI-anchored proteins is studied on the major blood cell populations ...
Paroxysmal Nocturnal Haemoglobinuria (PNH) is an acquired hematopoietic stem-cell disorder related to the somatic mutation in PIG-A gene (X-chromosome). This genetic alteration results in partial or total deficiency of all proteins normally linked to the cell membrane by glycosylphosphatidyl-inositol (GPI). Flow cytometry provides an efficient diagnostic test in which the lack of GPI-anchored proteins is studied on the major blood cell populations ...
... is a rare acquired, life-threatening disease of the blood. The disease is characterized by destruction of red blood cells (hemolytic anemia), blood clots (thrombosis), and impaired bone marrow function (not making enough of the three blood components). PNH affects 1-1.5 persons per million of the population and is primarily a disease of younger adults. The median age of diagnosis is 35-40 years of age, with occasional cases diagnosed in childhood or adolescence. PNH is closely related to aplastic anemia. In fact, up to 30% of newly diagnosed cases of PNH evolve from aplastic anemia. Similarly, the risk of developing PNH after treatment for aplastic anemia with immunosuppressive therapy (anti-thymocyte globulin and cyclosporine) is approximately 20-30%. The median survival after diagnosis is 10 years; however, some patients can survive for decades with only minor symptoms.. PNH occurs when mutations of a gene called PIG-A occur in a bone marrow stem cell. ...
Paroxysmal nocturnal hemoglobinuria (PNH) In this condition, the bone marrow--the soft spongy tissue that act as the blood manufacturing system for the entire body--produces defective red blood cells. The bodys natural defense system then destroys these defective red blood cells in a process is known as hemolysis.
The human complement system is part of the innate immune response that acts to eliminate pathogenic organisms. Complement is activated by three pathways leading to the sequential, non-enzymatic assembly of C5b, C6, C7, C8, and C9 to form the membrane attack complex (MAC). C6, C7, C8α, C8β, and C9 make up the
The term "nocturnal" refers to the belief that hemolysis is triggered by acidosis during sleep. However, this observation was later disproved. In individuals with paroxysmal nocturnal hemoglobinuria, hemolysis has been shown to occur throughout the day, but the urine concentrated overnight produces the dramatic change in color.[1] It is most noticeable in the morning, upon passing urine that has accumulated in the bladder during the night.[2] ...
Paroxysmal Nocturnal Hemoglobinuria - Epidemiology Insights to 2025 is a market research report available at US $2950 for a Single User PDF License from RnR Market Research Reports Library.
TY - JOUR. T1 - The membrane attack complex of complement. T2 - Relation of C7 to the metastable membrane binding site of the intermediate complex C5b-7. AU - Preissner, K. T.. AU - Podack, E. R.. AU - Muller-Eberhard, H. J.. PY - 1985/1/1. Y1 - 1985/1/1. N2 - Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent, C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization, C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing ...
Decay-accelerating factor (DAF) is a 70,000 Mr protein that has been isolated from the membrane of red cells. The function of DAF is to inhibit the assembly of amplifying enzymes of the complement cascade on the cell surface, thereby protecting them from damage by autologous complement. We raised monoclonal antibodies to DAF and used them to study its distribution in cells from the peripheral blood of normal individuals and of patients with paroxysmal nocturnal hemoglobinuria (PNH), a disease characterized by the unusual susceptibility of red cells to the hemolytic activity of complement. The results of immunoradiometric assays and of fluorescence-activated cell sorter analysis showed that DAF was present not only on red cells but was widely distributed on the surface membrane of platelets, neutrophils, monocytes, and B and T lymphocytes. By Western blotting, we observed small but consistent differences in the Mr of DAF from the membranes of various cell types. Quantitative studies showed that ...
Methods-This study was in 2 parts. First, male adult nude mice had an intracaudate injection of 30 μL saline, blood from male adult wild-type (WT) mice, or blood from CD47 knockout mice. Second, mice had an intracaudate injection of 30 μL CD47 knockout blood with clodronate or control liposomes. Clodronate liposomes were also tested in saline-injected mice. All mice then had magnetic resonance imaging to measure hematoma size and brain swelling. Brains were used for immunohistochemistry and Western blot. ...
GPI-Anchored Proteins. The majority of eukaryotic cell membrane proteins have hydrophobic amino acids stretches that consists of a transmembrane polypeptide chain, which embeds the proteins into phospholipids double layer of the membrane [18]. GPI anchored proteins are membrane bound proteins. Several proteins are linked to the outer cell membrane leaflet by GPI anchor. This structure involves three key elements: a core containing a phosphatidylinositol (PI) moiety, one glucosamine and three mannose molecules and one ethanolamine phosphate unit [19]. A peptide bond links the C-terminus of the protein polypeptide to the last moiety. The GPI-anchor is created in the endoplasmic reticulum and attached to the polypeptide post-translational by a transaminase enzyme [20-21]. Molecular Genetic Background. Until date, all PNH patients have had genetic mutations in an X-linked gene known as PIG-A [22, 23,9]. The PIG-A gene product is initially required in the assembly of GPI anchors [24]. Consequently, a ...
NEW HAVEN, Conn.--(BUSINESS WIRE)--Alexion Pharmaceuticals, Inc. (NASDAQ: ALXN) announced today that the pivotal Phase 3 study of ALXN1210, the Companys investigational long-acting C5 complement inhibitor, demonstrated non-inferiority to Soliris® (eculizumab) in complement inhibitor treatment-naïve patients with paroxysmal nocturnal hemoglobinuria (PNH) based on the co-primary endpoints of transfusion avoidance and normalization of lactate dehydrogenase (LDH) levels, a direct marker of complement-mediated hemolysis in PNH.
Coxsackieviruses- non-enveloped viruses that cause neurologic and cardiac disease in humans)- interact with at least two receptors during virus infection- CAR (the coxsackievirus and adenovirus receptor), and DAF (CD55, a complement regulatory molecule). On polarized epithelial cells, which are likely the first targets of natural infection, CAR is sequestered in intercellular junctions, and is inaccessible to virus; in contrast, DAF is expressed on the cell surface. We have found that DAF-mediated signals are important for virus infection of polarized cells. We are interested in defining the signaling molecules and other cellular factors required for coxsackievirus infection of polarized cells, and the mechanisms by which other viruses infect these cells. We are studying the cell biology of virus entry, with a focus on understanding the separate roles of the two receptors during the entry process. We have also developed transgenic and conditional knockout systems with which to examine the ...
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Patients of any age, including minors, with a diagnosis of PNH or a detected PNH clone, including patients previously treated with Soliris and withdrawn from treatment. Patients who are minors must have parent/legal guardian consent and must be willing and able to give assent, if applicable as determined by the Ethics Committees/Institutional Review Boards. Upon attaining adulthood, these patients must be re-consented ...
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I believe that a story is the shortest distance between two people. While this is my story, it is not just mine, and I did not do any of this alone. In April 1983, my husband Joe and I were 25 years old and attending to the required pre-marital blood work. Next thing we knew, we were sitting in a doctors office because my blood counts were abnormally low. They told us there was something wrong, but they didnt know what it was. ...
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Results At baseline, vWF, sVCAM-1, the EMP count, and F1+2 and D-dimer levels were significantly elevated in the patients, including those with no history of clinical thrombosis. Treatment with eculizumab was associated with significant decreases in plasma markers of coagulation activation (F1+2, p=0.012, and D-dimers, p=0.01), and reactional fibrinolysis (P-AP, p=0.0002). Eculizumab treatment also significantly reduced plasma markers of endothelial cell activation (t-PA, p=0.0005, sVCAM-1, p,0.0001, and vWF, p=0.0047) and total (p=0.0008) and free (p=0.0013) TFPI plasma levels. ...
Isolated C7 (m.w. 120,000) in 1% deoxycholate (DOC) forms dimers with an apparent m.w. of 230,000 and a DOC-binding capacity of 82 mol per mol of dimer. Dimerization of C7 also occurs in the presence of DOC-phospholipid mixed micelles and eventuates in the insertion of C7 dimers into the lipid bilayer upon the removal of the detergent. C5b-7 complex formation in the fluid phase or on lipid vesicles likewise involves polymerization. C5b-7 sedimented with 17-40S, which suggests a dimeric to hexameric composition. In avidin-biotin binding experiments in which two differentially labeled forms of C5b,6 (biotinyl 125I-C5b,6, and 131I-C5b,6) were used in equimolar amounts to assemble C5b-7, more than 50% of the biotinyl 125I-C5b,6-containing complexes also contained 131I label; again suggesting that C5b-7 consisted of oligomers rather than monomers. The conformation of C7 in C5b-7 and in dimeric C7 appeared similar by the following criteria. On formation of C5b-7 from C5b,6 and C7, a 20% increase in ...
Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal hematopoietic stem cell disorder with its protean clinical manifestations. This is due to partial or complete absence of glycophosphatidyl-inositol-anchor proteins (GPI-AP). The main aim of this review is to highlight various diagnostic modalities available, basic principle of each test and recent advances in the diagnosis of PNH. Recently among various tests available, the flow cytometry has become the gold standard for PNH testing. In order to overcome the difficulties encountered by the testing and research laboratories throughout the world, International Clinical Cytometry Society has come up with guidelines regarding the indications for testing, protocol for sample collection, processing, panel of antibodies as well as gating strategies to be used, how to interpret the test and reporting format to be used ...
infections; (ii) specific antibodies detected by conventional serology (CS) with epimastigote extracts, fixed trypomastigotes or other parasite antigens may circulate years after parasite elimination; (iii) functional antibodies are evidenced by complement-mediated lysis of freshly isolated trypomastigotes, a test which is 100% specific, highly sensitive, and the first to revert after T. cruzi elimination and (iv) the parasite target for the lytic antibodies is a glycoprotein of high molecular weight (gp160) anchored at the parasite surface. The complement regulatory protein has been cloned, sequenced and produced as a recombinant protein by other groups and is useful for identifying functional anti-T. cruzi antibodies in ELISA tests, thus dispensing with the need for live trypomastigotes to manage treated patients. If used instead of CS to define cures for Chagas patients, ELISA will avoid unnecessary delays in finding anti-T. cruzi drugs. Other highly sensitive techniques for parasite DNA ...
ARIUS Research (Roche) was developing monoclonal antibodies directed against the complement inhibitory protein CD59 for the treatment of cancer. CD59 blocks the
Species, Articles from Journal RESEARCH, Scientific Experts, Research Topics, Publications, Research Grants, Genomes and Genes about paroxysmal hemoglobinuria
Mouse anti Rat CD11a antibody, clone WT.1 reacts with rat CD11a, a glycoprotein of 160-170 kDa, associated with CD18. CD11a is one of the
Mouse anti Rat CD45 antibody, clone OX-29 recognizes rat CD45, also known as Receptor-type tyrosine-protein phosphatase C, Leukocyte commo
Quantity100 testsVolume2ImmunogenThymocytes and T lymphocytesBackground InformationCD59 (Protectin) is a small (18-20 kDa) GPI-anchored ubiquitousl...
An immune-based approach to allow antibodies in the plasma of HIV-1-infected individuals to regain their activity of antibody-dependent complement-mediated lysis (2010 ...
... - Hemoglobinuria paroxística nocturna ,, Hemólisis intravascular microangiopática 31 l Hiperglicemia, verglucemia Hiperinsulinismo. se distingue por el
In paroxysmal nocturnal hemoglobinuria (PNH) the loss of iron in the urine in the form of hemoglobin or hemosiderin is primarily responsible for the unusually high incidence of iron deficiency that has been observed (1, 2). Although repletion of iron stores may result in significant improvement in the anemia of PNH, therapeutic replacement of iron can also constitute a special problem in this disease since iron administration may accelerate hemolytic activity (1, 3).. This relationship between iron and PNH hemolytic activity was demonstrated in a patient whom we have studied recently. His case was of particular interest since the iron ...
During sublytic complement attack on human neutrophils, plasma-membrane vesicles are shed from the cell surface as a cell-protection mechanism. By using surface-iodinated neutrophils it was found that less than 2% of surface label was recovered in shed vesicles under conditions where 40% of complement component C9 was shed. SDS/PAGE of 125I-labelled shed vesicles and plasma membranes showed differences in iodination pattern, demonstrating the sorting of membrane proteins into the shed vesicles. Analysis of 32P-labelled phospholipids after labeling of neutrophils with [32P]Pi before sublytic complement attack showed the presence of phosphatidic acid, phosphatidylcholine, phosphatidyl-ethanolamine, phosphatidylinositol and polyphosphoinositides in shed vesicles. Quantitative analysis using [3H]acetic anhydride-labelling method showed that the molar proportions of phosphatidylethanolamine, phosphatidylinositol, phosphatidylserine and sphingomyelin were the same in shed vesicles as in plasma ...
Membrane cofactor protein (MCP) is a complement regulatory protein that is expressed on human cells and cell lines as two relatively broad species with Mr of 58,000-68,000 and 48,000-56,000. The structure of a previously reported cDNA clone indicated that MCP was a type 1 membrane glycoprotein and a member of the regulators of complement activation gene/protein cluster. However, it did not provide an explanation for the unusual phenotypic pattern of MCP. Therefore, in parallel with an analysis of the gene, additional cDNAs were cloned and characterized. Six different MCP cDNA classes were identified. All encode the same 5 untranslated signal peptide, four SCRs, transmembrane domain, and basic amino acid anchor. However, they differ in the length and composition of an extracellular serine/threonine/proline (STP)-rich area, a site of heavy O-glycosylation, and cytoplasmic tail. Analysis of the MCP gene demonstrated that the variation in cDNA structure was a result of alternative splicing. ...
Alloantibodies in pre-sensitized transplant candidates deposit complement membrane attack complexes (MAC) on graft endothelial cells (ECs), increasing risk of CD8+ T cell-mediated acute rejection. We recently showed (a) human ECs endocytose MAC into Rab5+ endosomes, creating a signaling platform that stabilizes NF-κB-inducing kinase (NIK) protein; (b) endosomal NIK activates both non-canonical NF-κB signaling to synthesize pro-IL-1β and an NLRP3 inflammasome to process and secrete active IL-1β; and (c) IL-1β activates ECs, increasing recruitment and activation of alloreactive effector memory CD4+ T (TEM) cells. Here, we report IFN-γ priming induced nuclear expression of IL-15/IL-15Rα complexes in cultured human ECs and that MAC-induced IL-1β stimulated translocation of IL-15/IL-15Rα complexes to the EC surface in a canonical NF-κB-dependent process, where IL-15/IL-15Rα transpresentation increased activation and maturation of alloreactive CD8+ TEM. Blocking NLRP3 inflammasome assembly, ...
Forty strains of Aeromonas hydrophila and Aeromonas veronii recovered from invasive and non-invasive infections were tested for their susceptibility to complement-mediated lysis by 65% pooled human serum (PHS). Based upon the results of this assay, two major populations could be defined. The first group (n = 20) consisted of serogroup 0:11 strains, all of which possessed a paracrystalline surface layer (S layer); all of these strains were refractory to the bactericidal activity of 65% PHS with the exception of A. hydrophila strain AH-121, which was composed of mixed subpopulations of serum-susceptible and serum-resistant clones. A second collection of isolates (n = 20), all of which were S-layer-negative, contained a subgroup of strains (n = 7) that were highly susceptible to complement-mediated lysis, showing a greater than 100-fold reduction of viable progeny within 30 min of exposure to 65% PHS. Serum-resistant strains from both groups could not be lysed by exposure of bacterial cells to polyclonal
Herein reported is the case of a 15-year-old female without a relevant medical history, who developed severe headaches, speech problems, dizziness, weakness, inability to walk, depressed consciousness, confusion, amnesia and vomiting, 14 days after receiving her first qHPV vaccine injection. After the second vaccine booster, her symptoms worsened and she expired 15 days later. Autopsy revealed cerebral oedema and cerebellar herniation indicative of a focally disrupted blood-brain barrier.. There was no evidence of an active brain infection. Immunohistochemistry (IHC) examination of the brainstem, hippocampus and the cerebellum showed prominent infiltration of T-lymphocytes and macrophages in all brain areas examined. Notably, marked activation of the complement membrane attack complex (MAC) was detected in the cerebellar Purkinje cells, hippocampal neurons and portions of the brainstem. This pattern of MAC activation in the absence of an active brain infection indicates an abnormal triggering of ...
Specimen must arrive within 48 hours of draw. Specimen must arrive by 1800 on Friday and 1 day before a holiday.. EDTA and sodium heparin whole blood are required.. Specimen Type: Whole blood. Container/Tube: Lavender top (EDTA). Specimen Volume: Full tube. Specimen Minimum Volume: 1 mL or 5 mL if 1 tube is submitted (Testing can be performed on either EDTA or sodium heparin whole blood if only 1 tube with is submitted with sufficient volume.). Specimen Type: Whole blood. Container/Tube: 10-mL dark-green top (sodium heparin). Specimen Volume: Full tube. Specimen Minimum Volume: 5 mL or 5 mL if 1 tube is submitted (Testing can be performed on either EDTA or sodium heparin whole blood if only 1 tube with is submitted with sufficient volume.). ...
Background-The cause of inflammatory bowel disease (IBD) is unknown, and it is often difficult to obtain diagnostic histological specimens. In considering the diagnosis of IBD, other causes of enteritis should be excluded. We present a case that illustrates this.. Case report-A 32 year old man presented with a history of intermittent diarrhoea, vomiting, colicky abdominal pain, and weight loss. There was no history of foreign travel or recent contact with gastroenteritis, and he had no family history or past medical history of note. On examination, he was a pale thin man with central abdominal tenderness; other systems were unremarkable. Abnormal blood tests included a raised white cell count 20.4 × 106/l (normal 4-11 × 106), C-reactive protein (CRP) 246 mg/l (normal 1-6 mg/l), and ferritin 310 μg/l (normal 12-1200 μg/l). Stool cultures were negative for pathogenic organisms. Colonoscopy revealed patchy chronic inflammatory infiltration in the lamina propria and enteroscopy showed active ...
Paroxysmal cold hemoglobinuria is a hemolytic syndrome. Hemolysis most commonly occurs intravascularly, after the antibody has passed through a cell attachment phase in the lower temperatures of the peripheral circulation.. The Donath-Landsteiner cold hemolysin is an unusual IgG antibody with anti-P specificity that was originally noted in cases of congenital or acquired syphilis. The disease it causes is termed "paroxysmal cold hemoglobinuria".. The intravascular hemolysis is due to the unusual complement-activating efficiency of this IgG antibody. As its name implies, this antibody is associated with cold hemoglobinuria. This antibody, although uncommon, is most frequently found in children with viral infections. Hemolysis, even though sometimes severe, is usually mild and tends to resolve as the infection clears.. ...
BOSTON--(BUSINESS WIRE)-- Alexion Pharmaceuticals, Inc. (NASDAQ:ALXN) today announced that Japans Ministry of Health, Labour and Welfare (MHLW) has approved ULTOMIRIS® (ravulizumab), the first and only long-acting C5 complement inhibitor administered every eight weeks, for the treatment of adult patients with paroxysmal nocturnal hemoglobinuria (PNH).
What: Shares of Alnylam Pharmaceuticals (NASDAQ:ALNY) were trading nearly 10% lower at 10:00 a.m. Monday after the company presented updated clinical data on two of its investigational compounds at the ongoing American Society of Hematology meeting.. So what: On Sunday the company gave an update on its ongoing Phase 1/2 trial of ALN-CC5, a compound being tested as a potential treatment for Paroxysmal Nocturnal Hemoglobinuria, or PNH. The results of the trial showed that ALN-CC5 achieved up to a 99% knockdown of Serum C5 levels and up to a 98% inhibition of Serum Hemolytic activity.. Those results managed to meet the companys goal of an 80% reduction in serum hemolytic activity and Alnylam management team believes that ALN-CC5 showed enough durability to possibly support a monthly, or even quarterly, dose regimen. The company will be transitioning the study to include patients with PNH by the end of this year and it plans on providing updated clinical data from this study by mid-2016.. In a ...
Amyndas Pharmaceuticals is a fast-developing innovator and emerging leader in the field of "complement therapeutics" developing advanced therapies to treat several human diseases including paroxysmal nocturnal hemoglobinuria, age-related macular degeneration, chronic inflammation during hemodialysis, ischemia-reperfusion injury and graph rejections.. ...
The complement system (Chap. 308) consists of a group of serum proteins functioning as a cooperative, self-regulating cascade of enzymes that adhere to- and in some cases disrupt-the surface of invading organisms. Some of these surface-adherent proteins (e.g., C3b) can then act as opsonins for destruction of microbes by phagocytes. The later, "terminal" components (C7, C8, and C9) can directly kill some bacterial invaders (notably, many of the neisseriae) by forming a membrane attack complex and disrupting the integrity of the bacterial membrane, thus causing bacteriolysis. ...
Membrane attack complex (MAC) is formed under the combined stimulation of amyloid beta (Aβ) and normal human serum (NHS), immunolabeled with a monoclonal mouse anti-human C5b-9 antibody and subsequently visualized by Cy3 (red). RPE cell nuclei are counter-stained with DAPI. Scale bars: 20 μm. See full article online. Read More ...
Dr. Elias Reichel, of Tufts University School of Medicine and a founder of Hemera Biosciences, Inc., of Boston, MA, presented on a new approach to treating the dry form of age-related macula degeneration. His paper was based on the research being done by Hemera Biosciences on HMR59, a naturally occurring protein that protects retinal cells from damage by MAC (Membrane Attack Complex), that can be delivered for long-lasting activity via a gene therapy approach. ...
For H&K P2000sk Sub-Compact, the Don Hume H721 Open Top is a high riding, canted, outside the waistband leather holster. The H721OT is excellent for concealment and all day carry. This design features a slide guard to provide comfort by protectin
高い抗原親和性、特異性と安定した品質を兼ね備えたアブカムのウサギ・モノクローナル抗体 RabMAb® ab109185 交差種: Hu 適用: WB,IP,IHC-P,Flow Cyt,ICC/IF
article{7a504027-4d4c-4bd8-8e6b-cd8a091bc4e1, abstract = {The Gram-positive bacterium Streptococcus pneumoniae is a major human pathogen that causes infections ranging from acute otitis media to life-threatening invasive disease. Pneumococci have evolved several strategies to circumvent the host immune response, in particular the complement attack. The pneumococcal glycolytic enzyme phosphoglycerate kinase (PGK) is both secreted and bound to the bacterial surface and simultaneously binds plasminogen and its activator tPA. In the present study, we demonstrate that PGK has an additional role in modulating the complement attack. PGK interacted with the membrane attack complex (MAC) components C5, C7 and C9, thereby blocking the assembly and membrane insertion of MAC resulting in significant inhibition of the hemolytic activity of human serum. Recombinant PGK interacted in a dose-dependent manner with these terminal pathway proteins, and the interactions were ionic in nature. In addition, PGK ...
Patients with paroxysmal nocturnal hemoglobinuria (PNH) have a clonal population of blood cells deficient in glycosylphosphatidylinositol-anchored (GPI-anchored) proteins, resulting from a mutation in the X-linked gene PIGA. Here we report on a set of patients in whom PNH results instead from biallelic mutation of PIGT on chromosome 20. These PIGT-PNH patients have clinically typical PNH, but they have in addition prominent autoinflammatory features, including recurrent attacks of aseptic meningitis. In all these patients we find a germ-line point mutation in one PIGT allele, whereas the other PIGT allele is removed by somatic deletion of a 20q region comprising maternally imprinted genes implicated in myeloproliferative syndromes. Unlike in PIGA-PNH cells, GPI is synthesized in PIGT-PNH cells and, since its attachment to proteins is blocked, free GPI is expressed on the cell surface. From studies of patients leukocytes and of PIGT-KO THP-1 cells we show that, through increased IL-1β ...
Purpose: : Uncontrolled activation of the alternative complement pathway is thought to be associated with age-related macular degeneration (AMD). Previously, we have shown that in retinal pigmented epithelium (RPE) monolayers, oxidative stress reduced complement inhibitor expression and function on the cell surface, resulting in sublytic activation of the membrane attack complex . Here we examined the potential ligand and pathway(s) involved in initiating complement-dependent RPE cell damage by oxidative stress. Methods: : ARPE-19 cells were grown as monolayers on transwell plates. Sublytic complement activation was induced by challenging monolayers with H2O2 in the presence of complement-sufficient normal human serum (NHS). Since sublytic complement activation results in VEGF release, which in turn reduces barrier function, transepithelial electrical resistance (TER) measurements were used as a measure of cell injury. Results: : (1) TER deteriorated rapidly in H2O2-exposed monolayers upon ...
Decay-accelerating factor (DAF), extracted from the stroma of human erythrocytes, was purified to homogeneity and incorporated into the membrane of sheep red cell complement intermediates, where its functional properties were analyzed. Incorporation of DAF into the cell membranes was temperature dependent, took place on pronase- or trypsin-treated erythrocytes, and did not depend on prior deposition of antibody, C1 or C4. Serum lipoproteins (high and low density) effectively inhibited DAF incorporation, but had no effect on the activity of DAF after its association with the cell membrane. The incorporated DAF could not be removed from the red cell surface by repeated washings in the presence of high salt concentration but was solubilized when the stroma were extracted with 0.1% Nonidet P-40. The presence of DAF in the membrane of EA did not affect the deposition of C1 and C4, but as few as 10(2) DAF molecules per cell profoundly inhibited the assembly of C3 and C5 convertases of both the ...
In vitro studies have proved the presence of epitopes of CD59 in the surface of trophozoites of Entamoeba histolytica (E. histolytica). However, it has not been proved if CD59 molecules are expressed in the surface during the trophozoites tissue invasion. The aim of the present study was to determine whether the complement-regulatory protein CD59 is present on trophozoites of E. histolytica in human colon. Eleven specimens of amoebic colitis were studied by immunohistochemistry and electron microscopy techniques with a monoclonal antibody against human CD59 molecule. Our results show that a CD59-like molecule is expressed in trophozoites of E. histolytica found in colonic amebic lesions. Also, a CD59-like molecule was detected by western blot analysis in whole lysate of E. histolytica as well as on the plasma membrane by immunocytochemistry. These results suggest that E. histolytica can use CD59-like protein against the lytic action of membrane attack complex.

CD59 antigen - WikipediaCD59 antigen - Wikipedia

CD59 antigen (also called 1F-5Ag, H19, HRF20, MACIF, MIRL, P-18 or protectin) inhibits formation of membrane attack complex ( ... CD molecules are leucocyte antigens on cell surfaces. CD antigens nomenclature is updated at Protein Reviews On The Web (http ... IPR003631 Cell-surface glycoprotein Ly-6/CD59 InterPro: IPR003632 ARS[disambiguation needed]; CD177; CD59; LY6D; LY6E; LY6H; ... Genetic defects in GPI-anchor attachment that cause a reduction or loss of both CD59 and CD55 on erythrocytes produce the ...
more infohttps://en.wikipedia.org/wiki/CD59_antigen

The CD59 antigen--a multifunctional molecule. - Oxford NeuroscienceThe CD59 antigen--a multifunctional molecule. - Oxford Neuroscience

Animals, Animals, Genetically Modified, Antigens, CD, CD59 Antigens, Chromosomes, Human, Pair 11, Complement Membrane Attack ...
more infohttps://www.neuroscience.ox.ac.uk/publications/17362

Cell surface regulators of complement, 5I2 antigen, and CD59, in the rat eye and adnexal tissues. | IOVS | ARVO JournalsCell surface regulators of complement, 5I2 antigen, and CD59, in the rat eye and adnexal tissues. | IOVS | ARVO Journals

CONCLUSIONS: 5I2 antigen and rat CD59 are expressed in high levels and distributed similarly in the rat eye and lacrimal gland ... D S Bardenstein, C Cheyer, N Okada, B P Morgan, M E Medof; Cell surface regulators of complement, 5I2 antigen, and CD59, in the ... The retina showed labeling at multiple levels, with that of rat CD59 being more intense than that of 5I2 antigen. The lacrimal ... Corneal endothelial cells showed intense labeling for rat CD59 but not for 5I2 antigen. The iris and ciliary body showed ...
more infohttps://iovs.arvojournals.org/article.aspx?articleid=2181374

CD59 blockade enhances antigen-specific CD4+ T cell responses in humans: a new target for cancer immunotherapy?  -ORCACD59 blockade enhances antigen-specific CD4+ T cell responses in humans: a new target for cancer immunotherapy? -ORCA

CD59 blockade enhances antigen-specific CD4+ T cell responses in humans: a new target for cancer immunotherapy? The Journal of ... CD59 blockade enhances antigen-specific CD4+ T cell responses in humans: a new target for cancer immunotherapy? ... In this study, we explored the role of CD59 on human CD4+ T cells. Our data demonstrate that CD59 is up-regulated on activated ... CD59, a broadly expressed GPI-anchored molecule, regulates formation of the membrane attack complex of the complement cascade. ...
more infohttp://orca-mwe.cf.ac.uk/29596/

Effects of CD59 on antitumoral activities of phycocyanin from Spirulina platensis.Effects of CD59 on antitumoral activities of phycocyanin from Spirulina platensis.

CD59) gene expression of Hela cells and antitumoral mechanism of PC was investigated in this study. PC was purified by ... 0/Antigens, CD59; 0/Antigens, CD95; 0/Antineoplastic Agents; 0/FAS protein, human; 0/RNA, Messenger; 0/Receptors, Tumor ... Antigens, CD59 / genetics, metabolism*, pharmacology. Antigens, CD95. Antineoplastic Agents / isolation & purification, ... The CD59 cDNA was inserted into the eukaryotic expression plasmid pALTER-MAX, and the recombinant vector pALTER-MAX-CD59 was ...
more infohttp://www.biomedsearch.com/nih/Effects-CD59-antitumoral-activities-phycocyanin/16271846.html

LY6D Gene - GeneCards | LY6D Protein | LY6D AntibodyLY6D Gene - GeneCards | LY6D Protein | LY6D Antibody

Lymphocyte Antigen 6 Family Member D, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards ... The human E48 antigen, highly homologous to the murine Ly-6 antigen ThB, is a GPI-anchored molecule apparently involved in ... lymphocyte antigen complex,member D,homolog with the murine LY-6 family members of small cysteine-rich proteins,expressed in ... LY6D (Lymphocyte Antigen 6 Family Member D) is a Protein Coding gene. Diseases associated with LY6D include Inferior Myocardial ...
more infohttps://www.genecards.org/cgi-bin/carddisp.pl?gene=LY6D

KEGG BRITE: CD Molecules - Homo sapiens (human)KEGG BRITE: CD Molecules - Homo sapiens (human)

CD58 antigen K04008 CD59; CD59 antigen K06493 ITGB3; integrin beta 3 K06494 SELE; selectin, endothelial cell K06495 SELL; ... CD79A antigen K06507 CD79B; CD79B antigen K05412 CD80; CD80 antigen K06508 CD81; CD81 antigen K06509 KAI1; CD82 antigen K06510 ... CD300 antigen K06719 CD300; CD300 antigen K06719 CD300; CD300 antigen K06719 CD300; CD300 antigen K06721 CLEC10A; C-type lectin ... 966 CD59; CD59 molecule (CD59 blood group) 3690 ITGB3; integrin subunit beta 3 6401 SELE; selectin E 6402 SELL; selectin L 6403 ...
more infohttps://www.genome.jp/kegg-bin/get_htext?hsa04090+4486

Role of Complement in Xenograft Rejection | SpringerLinkRole of Complement in Xenograft Rejection | SpringerLink

Cytoprotective effect of CD59 antigen on xenotransplantation immunity. Transplant. Proc. 24, 485, 1992PubMedGoogle Scholar ... Cowan, P.J., Witort, E., Barlow, H., Pearse, M.J., dApice, A.J.F. Expression of CD59 in transgenic mice using the human ICAM-2 ... Meri, S. Protectin (CD59). Complement lysis inhibitor and prototype domain in a new protein superfamily. The Immunologist. 2, ... Zhao, J., Rollins, S.A., Maher, S.E., Bothwell, A.L., Sims, P.J. Amplified gene expression in CD59-transfected Chinese hamster ...
more infohttps://link.springer.com/chapter/10.1007/978-3-642-60572-7_6

PLAUR - Urokinase plasminogen activator surface receptor - Homo sapiens (Human) - PLAUR gene & proteinPLAUR - Urokinase plasminogen activator surface receptor - Homo sapiens (Human) - PLAUR gene & protein

IPR018363 CD59_antigen_CS. IPR016054 LY6_UPA_recep-like. IPR033084 U-PAR. ... IPR018363 CD59_antigen_CS. IPR016054 LY6_UPA_recep-like. IPR033084 U-PAR. ... Urokinase plasminogen activator surface receptor, U-PAR, uPAR (Monocyte activation antigen Mo3) (CD antigen CD87) ...
more infohttps://www.uniprot.org/uniprot/M0R1I2

Code System ConceptCode System Concept

Lymphocyte antigen CD59 (substance). Code System Preferred Concept Name. Lymphocyte antigen CD59 (substance). ...
more infohttps://phinvads.cdc.gov/vads/ViewCodeSystemConcept.action?oid=2.16.840.1.113883.6.96&code=87661004

NIOSHTIC-2  Publications Search - 20041729 - Bone mineralization and inflammation genes increase in muscles as a consequence of...NIOSHTIC-2 Publications Search - 20041729 - Bone mineralization and inflammation genes increase in muscles as a consequence of...

CD59 antigen, complement component factor h); and 3) task performance in aged rats only (corticotropin releasing hormone, ... interleukin 4, interferon regulatory factor 1, inhibin alpha, and interleukin 6). Also, CD4 antigen, IL-4 and IL-10 mRNA ...
more infohttps://www.cdc.gov/niosh/nioshtic-2/20041729.html

leukemia adult acute myelogenous stage drug therapy 2000:2010[pubdate] *count=100 - BioMedLib™ search engineleukemia adult acute myelogenous stage drug therapy 2000:2010[pubdate] *count=100 - BioMedLib™ search engine

Chemical-registry-number] 0 / Antigens, CD59; 0 / Membrane Proteins; 0 / P-Glycoprotein; 0 / phosphatidylinositol glycan-class ... Chemical-registry-number] 0 / HLA-B Antigens; 0 / HLA-B16 antigen; 0 / HLA-DR6 Antigen; 0 / Immunosuppressive Agents; 83869-56- ... Antigens, CD59 / analysis. Bone Marrow / pathology. Cytogenetic Analysis. Female. Frameshift Mutation. Humans. ... HLA-B Antigens / immunology. HLA-DR6 Antigen / immunology. Hodgkin Disease / drug therapy. Hodgkin Disease / immunology. ...
more infohttp://www.bmlsearch.com/?kwr=leukemia+adult+acute+myelogenous+stage+drug+therapy+2000:2010%5Bpubdate%5D&cxts=100&stmp=b1

CD59 - Beckman CoulterCD59 - Beckman Coulter

The CD59 antigen, also known as Protectin or Membrane Inhibitor of Reactive Lysis (MIRL) is a 18-20 kDa, single-chain, ... CD59 Antigen. The CD59 antigen, also known as Protectin or Membrane Inhibitor of Reactive Lysis (MIRL) is a 18-20 kDa, single- ... CD59 inhibits complement lysis by binding to the C5b-8 and C5b-9 complexes and thus preventing formation of the polymeric C9 ... mediated lysis suggest that viruses incorporate host cell-derived C regulatory proteins such as CD59 and CD55, a mechanism by ...
more infohttps://www.mybeckman.ca/reagents/coulter-flow-cytometry/antibodies-and-kits/single-color-antibodies/cd59

CD59 and Ly6E sequence comparison. Mature protein seque | Open-iCD59 and Ly6E sequence comparison. Mature protein seque | Open-i

CD59 and Ly6E sequence comparison. Mature protein sequences are shown with the conserved cysteine residues marked (:). The ... Mouse Ly6E antigen (18) is a structural but not functional analogue of CD59 (see Fig. 1). In the approach reported here, ... Mentions: CD59 belongs to the Ly6 superfamily of proteins which includes functional CD59 analogues from other species, snake ... Mentions: CD59 belongs to the Ly6 superfamily of proteins which includes functional CD59 analogues from other species, snake ...
more infohttps://openi.nlm.nih.gov/detailedresult.php?img=PMC2196154_JEM.yu1&req=4

Molecule InformationMolecule Information

Human Leucocyte Differentiation Antigens) Workshops and names and characterises CD molecules. ... GENE_NAME : CD59. CD_NAME : CD59. DESC: CD59 antigen p18-20. OTH_NAMES: MGC2354; MIC11; MIN1; MIN2; MIN3; MSK21; PROTECTIN ...
more infohttp://hcdm.org/index.php/molecule-information?view=molecule&task=viewmolecule&moleculeid=305&search=

NIOSHTIC-2 Search Results - Full ViewNIOSHTIC-2 Search Results - Full View

CD59 antigen, complement component factor h); and 3) task performance in aged rats only (corticotropin releasing hormone, ... interleukin 4, interferon regulatory factor 1, inhibin alpha, and interleukin 6). Also, CD4 antigen, IL-4 and IL-10 mRNA ...
more infohttp://www2a.cdc.gov/nioshtic-2/BuildQyr.asp?s1=%27ergonom%2A%27+or+musculoskeletal+or+repetitive+or+carpal&f1=TI&Startyear=&t1=1&s2=%27ergonom%2A%27+or+musculoskeletal+or+repetitive+or+carpal&terms=3&Adv=1&ct=&B1=Search&f2=KW&Limit=500&Sort=DP+DESC&D1=10&EndYear=&PageNo=198&RecNo=1977&View=f&

Amino acid sequence alignment of CD59 and CD59 homologu | Open-iAmino acid sequence alignment of CD59 and CD59 homologu | Open-i

Amino acid sequence alignment of CD59 and CD59 homologues from different species. The conserved residues located in the groove ... Figure 6: Amino acid sequence alignment of CD59 and CD59 homologues from different species. The conserved residues located in ... Figure 6: Amino acid sequence alignment of CD59 and CD59 homologues from different species. The conserved residues located in ... Bottom Line: CD59 functions by binding to C8 and/or C9 in the nascent MAC and interfering with C9 membrane insertion and ...
more infohttps://openi.nlm.nih.gov/detailedresult.php?img=PMC2196154_JEM.yu6&req=4

Prostate stem cell antigen: A cell surface marker overexpressed in prostate cancer | PNASProstate stem cell antigen: A cell surface marker overexpressed in prostate cancer | PNAS

... proteins was confirmed by performing the same experiment on 293T cells transfected with the GPI-linked antigen CD59 or the non- ... stem cell antigen 2;. PLC,. phospholipase C;. PSCA,. prostate stem cell antigen;. GPI,. glycosylphosphatidylinositol. ... prostate-specific antigen;. PSMA,. prostate-specific membrane antigen;. RDA,. representational difference analysis;. RT-PCR,. ... Prostate stem cell antigen (PSCA) is a prostate-specific gene with 30% homology to stem cell antigen 2, a member of the Thy-1/ ...
more infohttps://www.pnas.org/content/95/4/1735?ijkey=6fec0b4f31c0cbac47904579c93af963e9ad6807&keytype2=tf_ipsecsha

RCSB PDB - 1ERG: THREE-DIMENSIONAL SOLUTION STRUCTURE OF THE EXTRACELLULAR REGION OF THE COMPLEMENT REGULATORY PROTEIN, CD59, A...RCSB PDB - 1ERG: THREE-DIMENSIONAL SOLUTION STRUCTURE OF THE EXTRACELLULAR REGION OF THE COMPLEMENT REGULATORY PROTEIN, CD59, A...

CD59, A NEW CELL SURFACE PROTEIN DOMAIN RELATED TO NEUROTOXINS ... The cell surface antigen CD59 is an inhibitor of complement- ... The cell surface antigen CD59 is an inhibitor of complement-mediated lysis and a member of the Ly6 superfamily (Ly6SF) of ... Three-dimensional solution structure of the extracellular region of the complement regulatory protein CD59, a new cell-surface ... THREE-DIMENSIONAL SOLUTION STRUCTURE OF THE EXTRACELLULAR REGION OF THE COMPLEMENT REGULATORY PROTEIN, CD59, A NEW CELL SURFACE ...
more infohttps://www.rcsb.org/structure/1ERG

Three-finger protein - WikipediaThree-finger protein - Wikipedia

Other LU proteins, such as the CD59 antigen, have well-studied functions in regulation of the immune system. Snake three-finger ... Other LU domain proteins are small globular proteins such as CD59 antigen, LYNX1, SLURP1, and SLURP2. Many LU domain containing ... The family is named for two representative groups of members, the small globular protein lymphocyte antigen 6 (LY6) family and ... "High-resolution structures of bacterially expressed soluble human CD59". Acta Crystallographica. Section F, Structural Biology ...
more infohttps://en.wikipedia.org/wiki/Three-finger_protein

CD59 Antibody (MEM-43) (NB500-330): Novus BiologicalsCD59 Antibody (MEM-43) (NB500-330): Novus Biologicals

Mouse Monoclonal Anti-CD59 Antibody (MEM-43). Validated: Flow, IHC, IHC-Fr, IHC-P, IP, B/N, CyTOF-ready. Tested Reactivity: ... CD59 antigen p18-20 (antigen identified by monoclonal antibodies 16.3A5, EJ16 ... Blogs on CD59. There are no specific blogs for CD59, but you can read our latest blog posts. ... Bioinformatics Tool for CD59 Antibody (NB500-330). Discover related pathways, diseases and genes to CD59 Antibody (NB500-330). ...
more infohttps://www.novusbio.com/products/cd59-antibody-mem-43_nb500-330

Michael Chorev | Harvard Catalyst Profiles | Harvard CatalystMichael Chorev | Harvard Catalyst Profiles | Harvard Catalyst

Cantel S, Kavishwar A, Schlimme M, Khatri A, Halperin JA, Chorev M. Glycated-CD59 antigen: exploration of synthetic approaches ... Hu W, Ge X, You T, Xu T, Zhang J, Wu G, Peng Z, Chorev M, Aktas BH, Halperin JA, Brown JR, Qin X. Human CD59 inhibitor ... Plasma Glycated CD59, a Novel Biomarker for Detection of Pregnancy-Induced Glucose Intolerance. Diabetes Care. 2017 07; 40(7): ... A specific and sensitive assay for blood levels of glycated CD59: a novel biomarker for diabetes. Am J Hematol. 2013 Aug; 88(8 ...
more infohttps://connects.catalyst.harvard.edu/Profiles/display/Person/78179

Yuzawa Yukio - Research Output
     - Fujita Health UniversityYuzawa Yukio - Research Output - Fujita Health University

CD59 protects rat kidney from complement mediated injury in collaboration with Crry. Watanabe, M., Morita, Y., Mizuno, M., ... In vivo gene transfer of endo-β-galactosidase C removes αGal antigen on erythrocytes and endothelial cells of the organs. Miki ... Antibody-mediated redistribution and shedding of endothelial antigens in the rabbit. Yuzawa, Y., Brentjens, J. R., Brett, J., ... Renal immune deposits induced by antibodies reactive with cell-surface antigens in laboratory animals and in man. Fukatsu, A., ...
more infohttps://pure.fujita-hu.ac.jp/en/persons/yukio-yuzawa/publications/?type=%2Fdk%2Fatira%2Fpure%2Fresearchoutput%2Fresearchoutputtypes%2Fcontributiontojournal%2Farticle&page=3

Assessing donor chimerism using flow cytometry in paroxysmal nocturnal haemoglobinuria after stem cell transplantation--a case...Assessing donor chimerism using flow cytometry in paroxysmal nocturnal haemoglobinuria after stem cell transplantation--a case...

Engrafted patients will show the presence of CD 55 and CD 59 on their red cells and white cells. We describe here the ... Engrafted patients will show the presence of CD 55 and CD 59 on their red cells and white cells. We describe here the ... Engrafted patients will show the presence of CD 55 and CD 59 on their red cells and white cells. We describe here the ... Engrafted patients will show the presence of CD 55 and CD 59 on their red cells and white cells. We describe here the ...
more infohttps://ukm.pure.elsevier.com/en/publications/assessing-donor-chimerism-using-flow-cytometry-in-paroxysmal-noct

CD59 antibody | acris-antibodies.comCD59 antibody | acris-antibodies.com

Rat CD59 was previously known as rat inhibitory protein (RIP) and it is a potent inhibitor of the complement membrane attack ... T8 antigen, T1 antigen, a monocyte antigen, and a pan-leucocyte antigen. Folia Biol (Praha). 1986;32(1):12-25. (original ... CD59 (transcript variant 2). Not available. Recombinant protein of human CD59 molecule, complement regulatory protein (CD59), ... Lenti ORF particles, CD59 (mGFP-tagged)-Human CD59 molecule, complement regulatory protein (CD59), transcript variant 1, 200 uL ...
more infohttps://www.acris-antibodies.com/target/cd59-antibody.htm?p=2
  • The CD59 antigen--a multifunctional molecule. (ox.ac.uk)
  • CD59, a broadly expressed GPI-anchored molecule, regulates formation of the membrane attack complex of the complement cascade. (cf.ac.uk)
  • We present data obtained from a combination of molecular modeling and mutagenesis techniques, which together indicate that the active site of CD59 is located in the vicinity of a hydrophobic groove on the face of the molecule opposite to a "hydrophobic strip" suggested earlier. (nih.gov)
  • Fig. 7 a displays the molecule in an orientation that shows that the regions of CD59 that can be replaced by Ly6E without loss of function (1-16 and 57-77) are located at the backside of the molecule (in yellow, Fig. 7 a). (nih.gov)
  • CD59 is a small (18 - 25 kDa) molecule, linked to the cell membrane through a glycosyl phosphatidylinositol (GPI) anchor and comprising 77 amino acids with a single N-linked carbohydrate group at Asn-18. (acris-antibodies.com)
  • CONCLUSIONS: 5I2 antigen and rat CD59 are expressed in high levels and distributed similarly in the rat eye and lacrimal gland to DAF, MCP, and MIRL in the human eye and lacrimal gland. (arvojournals.org)
  • Immunohistochemistry-Frozen: CD59 Antibody (MEM-43) [NB500-- Human tonsil frozen tissue section stained for CD59 (red) and counterstained with DAPI (blue). (novusbio.com)
  • The regulatory effect of phycocyanin (PC) from Spirulina platensis on cluster of differentiation 59 (CD59) gene expression of Hela cells and antitumoral mechanism of PC was investigated in this study. (biomedsearch.com)
  • 2. Stefanova I, Hilgert I, Kristofova H, Brown R, Low MG, Horejsi V.: Characterization of a broadly expressed human leucocyte surface antigen MEM-43 anchored in membrane through phosphatidylinositol. (acris-antibodies.com)
  • Genetic defects in GPI-anchor attachment that cause a reduction or loss of both CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal nocturnal hemoglobinuria (PNH). (wikipedia.org)
  • A distinctive histidine residue is essential for in vivo glycation-inactivation of human CD59 transgenically expressed in mice erythrocytes: Implications for human diabetes complications. (harvard.edu)
  • CD59 regulates the formation and function of the lytic C5b-9 complex by binding C8 and preventing the unfolding and membrane insertion of C9 and by binding C9 and restricting its polymerization. (acris-antibodies.com)
  • The CD59 cDNA was inserted into the eukaryotic expression plasmid pALTER-MAX, and the recombinant vector pALTER-MAX-CD59 was successfully constructed. (biomedsearch.com)
  • By using cationic liposome (Lipfectamine-2000)-mediated transfection method, the recombinant plasmid pALTER-MAX-CD59 and the selective marker PcDNA were cotransfected into Hela cells and normal Chinese hamster ovary (CHO) cells. (biomedsearch.com)
  • Prostate stem cell antigen (PSCA) is a prostate-specific gene with 30% homology to stem cell antigen 2, a member of the Thy-1/Ly-6 family of glycosylphosphatidylinositol (GPI)-anchored cell surface antigens. (pnas.org)
  • Another potential advantage to searching for membrane-bound tumor antigens is that they may provide insights into the biology of prostate cancer progression. (pnas.org)
  • Cell surface regulators of complement, 5I2 antigen, and CD59, in the rat eye and adnexal tissues. (arvojournals.org)
  • The amino acids forming the surface loops and helix of CD59 are shown. (nih.gov)
  • The active site was then further defined by a series of site-specific mutations, selected as a result of comparing evolutionary conserved residues and modeling of the molecular surface of CD59. (nih.gov)
  • The identification of cell surface antigens is critical to the development of new diagnostic and therapeutic modalities for the management of prostate cancer. (pnas.org)
  • Prostate specific membrane antigen (PSMA) is a recently described cell surface marker of prostate cancer currently being evaluated for the detection of metastatic cells and as a target for mAb and other immunological therapies ( 4 , 5 ). (pnas.org)
  • One promising candidate, prostate stem cell antigen (PSCA), is a prostate-specific cell surface antigen expressed strongly by both androgen-dependent and -independent LAPC-4 tumors. (pnas.org)
  • Rat astrocytes in vitro express CD59 on its surface. (acris-antibodies.com)
  • occurs singly in other GPI-linked cell-surface glycoproteins (Ly-6 family, CD59, thymocyte B cell antigen, Sgp-2). (embl.de)
  • The findings were striking and indicated that blockade of CD59 significantly enhanced the CD4+ T cell response to two different tumor Ags. (cf.ac.uk)
  • Our data demonstrate that CD59 is up-regulated on activated CD4+ T cells and serves to down-modulate their activity in response to polyclonal and Ag- specific stimulation. (cf.ac.uk)
  • These data highlight the potential for manipulating CD59 expression on T cells for boosting weak immune responses, such as those found in individuals with cancer. (cf.ac.uk)
  • CD59 is expressed on all haematopoietic cells and is widely expressed on cells in all tissues. (mybeckman.ca)
  • In rat, CD59 is expressed on vacular endothelium and circulating cells. (acris-antibodies.com)
  • In the central nervous system (CNS) of the rat, CD59 is expressed on the Schwann sheath of peripheral nerve fibres and on ependymal cells, but not on glial cells and neurons in the CNS. (acris-antibodies.com)
  • We previously demonstrated that mouse CD59 also down-modulates CD4+ T cell activity in vivo. (cf.ac.uk)