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Description:
Chemoattractant active on T-lymphocytes, monocytes, but not neutrophils. Activates the C-X-C chemokine receptor CXCR4 to induce a rapid and transient rise in the level of intracellular calcium ions and chemotaxis. Also binds to atypical chemokine receptor ACKR3, which activates the beta-arrestin pathway and acts as a scavenger receptor for SDF-1. SDF-1-beta(3-72) and SDF-1-alpha(3-67) show a reduced chemotactic activity. Binding to cell surface proteoglycans seems to inhibit formation of SDF-1-alpha(3-67) and thus to preserve activity on local sites. Acts as a positive regulator of monocyte migration and a negative regulator of monocyte adhesion via the LYN kinase. Stimulates migration of monocytes and T-lymphocytes through its receptors, CXCR4 and ACKR3, and decreases monocyte adherence to surfaces coated with ICAM-1, a ligand for beta-2 integrins. SDF1A/CXCR4 signaling axis inhibits beta-2 integrin LFA-1 mediated adhesion of monocytes to ICAM-1 through LYN kinase. Inhibits CXCR4-mediated infection by T-cell line-adapted HIV-1. Plays a protective role after myocardial infarction. Induces down-regulation and internalization of ACKR3 expressed in various cells. Has several critical functions during embryonic development; required for B-cell lymphopoiesis, myelopoiesis in bone marrow and heart ventricular septum formation.
Description:
This MAb specifically precipitates heterogeneous material of high MW, identified as perlecan, a major heparan-sulfate proteoglycan (HSPG) within all basement membranes and cell surfaces. It does not cross-react with laminin, fibronectin, or dermatran sulfate proteoglycan. Because of perlecan s strategic location and ability to store and protect growth factors, it has been strongly implicated in the control of tumor cell growth and metastatic behavior. Perlecan possesses angiogenic and growth-promoting attributes primarily by acting as a co-receptor for basic fibroblast growth factor (FGF-2). Suppression of perlecan causes substantial inhibition of neoplastic growth and neovascularization. Thus, perlecan is a potent inducer of neoplasm growth and angiogenesis in vivo and therapeutic interventions targeting this key modulator of tumor progression may improve neoplastic treatment.
Description:
This MAb specifically precipitates heterogeneous material of high MW, identified as perlecan, a major heparan-sulfate proteoglycan (HSPG) within all basement membranes and cell surfaces. It does not cross-react with laminin, fibronectin, or dermatran sulfate proteoglycan. Because of perlecan s strategic location and ability to store and protect growth factors, it has been strongly implicated in the control of tumor cell growth and metastatic behavior. Perlecan possesses angiogenic and growth-promoting attributes primarily by acting as a co-receptor for basic fibroblast growth factor (FGF-2). Suppression of perlecan causes substantial inhibition of neoplastic growth and neovascularization. Thus, perlecan is a potent inducer of neoplasm growth and angiogenesis in vivo and therapeutic interventions targeting this key modulator of tumor progression may improve neoplastic treatment.
Description:
Reacts with human CD59, a 20 kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). This MAb is useful for study on GPI-anchored proteins, PNH and CD59 functions. CD59 is widely distributed on cells in all tissues. The expression of CD59 on erythrocytes is important for their survival.
Description:
Reacts with human CD59, a 20 kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). This MAb is useful for study on GPI-anchored proteins, PNH and CD59 functions. CD59 is widely distributed on cells in all tissues. The expression of CD59 on erythrocytes is important for their survival.
Description:
Chemoattractant active on T-lymphocytes, monocytes, but not neutrophils. Activates the C-X-C chemokine receptor CXCR4 to induce a rapid and transient rise in the level of intracellular calcium ions and chemotaxis. Also binds to atypical chemokine receptor ACKR3, which activates the beta-arrestin pathway and acts as a scavenger receptor for SDF-1. SDF-1-beta(3-72) and SDF-1-alpha(3-67) show a reduced chemotactic activity. Binding to cell surface proteoglycans seems to inhibit formation of SDF-1-alpha(3-67) and thus to preserve activity on local sites. Acts as a positive regulator of monocyte migration and a negative regulator of monocyte adhesion via the LYN kinase. Stimulates migration of monocytes and T-lymphocytes through its receptors, CXCR4 and ACKR3, and decreases monocyte adherence to surfaces coated with ICAM-1, a ligand for beta-2 integrins. SDF1A/CXCR4 signaling axis inhibits beta-2 integrin LFA-1 mediated adhesion of monocytes to ICAM-1 through LYN kinase. Inhibits CXCR4-mediated infection by T-cell line-adapted HIV-1. Plays a protective role after myocardial infarction. Induces down-regulation and internalization of ACKR3 expressed in various cells. Has several critical functions during embryonic development; required for B-cell lymphopoiesis, myelopoiesis in bone marrow and heart ventricular septum formation.
Description:
Reacts with human CD59, a 20 kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). This MAb is useful for study on GPI-anchored proteins, PNH and CD59 functions. CD59 is widely distributed on cells in all tissues. The expression of CD59 on erythrocytes is important for their survival.
Description:
Chemoattractant active on T-lymphocytes, monocytes, but not neutrophils. Activates the C-X-C chemokine receptor CXCR4 to induce a rapid and transient rise in the level of intracellular calcium ions and chemotaxis. Also binds to atypical chemokine receptor ACKR3, which activates the beta-arrestin pathway and acts as a scavenger receptor for SDF-1. SDF-1-beta(3-72) and SDF-1-alpha(3-67) show a reduced chemotactic activity. Binding to cell surface proteoglycans seems to inhibit formation of SDF-1-alpha(3-67) and thus to preserve activity on local sites. Acts as a positive regulator of monocyte migration and a negative regulator of monocyte adhesion via the LYN kinase. Stimulates migration of monocytes and T-lymphocytes through its receptors, CXCR4 and ACKR3, and decreases monocyte adherence to surfaces coated with ICAM-1, a ligand for beta-2 integrins. SDF1A/CXCR4 signaling axis inhibits beta-2 integrin LFA-1 mediated adhesion of monocytes to ICAM-1 through LYN kinase. Inhibits CXCR4-mediated infection by T-cell line-adapted HIV-1. Plays a protective role after myocardial infarction. Induces down-regulation and internalization of ACKR3 expressed in various cells. Has several critical functions during embryonic development; required for B-cell lymphopoiesis, myelopoiesis in bone marrow and heart ventricular septum formation.
Description:
Acute phase-regulated receptor involved in clearance and endocytosis of hemoglobin/haptoglobin complexes by macrophages and may thereby protect tissues from free hemoglobin-mediated oxidative damage. May play a role in the uptake and recycling of iron, via endocytosis of hemoglobin/haptoglobin and subsequent breakdown of heme. Binds hemoglobin/haptoglobin complexes in a calcium-dependent and pH-dependent manner. Exhibits a higher affinity for complexes of hemoglobin and multimeric haptoglobin of HP*1F phenotype than for complexes of hemoglobin and dimeric haptoglobin of HP*1S phenotype. Induces a cascade of intracellular signals that involves tyrosine kinase-dependent calcium mobilization, inositol triphosphate production and secretion of IL6 and CSF1. Isoform 3 exhibits the higher capacity for ligand endocytosis and the more pronounced surface expression when expressed in cells. After shedding, the soluble form (sCD163) may play an anti-inflammatory role, and may be a valuable diagnostic parameter for monitoring macrophage activation in inflammatory conditions.
Description:
This antibody reacts with human CD59, a 20 kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. CD59 is widely distributed on cells in all tissues. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. The expression of CD59 on erythrocytes is important for their survival. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). It is useful for study on GPI-anchored proteins, PNH and CD59 functions.
Description:
Acute phase-regulated receptor involved in clearance and endocytosis of hemoglobin/haptoglobin complexes by macrophages and may thereby protect tissues from free hemoglobin-mediated oxidative damage. May play a role in the uptake and recycling of iron, via endocytosis of hemoglobin/haptoglobin and subsequent breakdown of heme. Binds hemoglobin/haptoglobin complexes in a calcium-dependent and pH-dependent manner. Exhibits a higher affinity for complexes of hemoglobin and multimeric haptoglobin of HP*1F phenotype than for complexes of hemoglobin and dimeric haptoglobin of HP*1S phenotype. Induces a cascade of intracellular signals that involves tyrosine kinase-dependent calcium mobilization, inositol triphosphate production and secretion of IL6 and CSF1. Isoform 3 exhibits the higher capacity for ligand endocytosis and the more pronounced surface expression when expressed in cells. After shedding, the soluble form (sCD163) may play an anti-inflammatory role, and may be a valuable diagnostic parameter for monitoring macrophage activation in inflammatory conditions.
Description:
This MAb specifically precipitates heterogeneous material of high MW, identified as perlecan, a major heparan-sulfate proteoglycan (HSPG) within all basement membranes and cell surfaces. It does not cross-react with laminin, fibronectin, or dermatran sulfate proteoglycan. Because of perlecan s strategic location and ability to store and protect growth factors, it has been strongly implicated in the control of tumor cell growth and metastatic behavior. Perlecan possesses angiogenic and growth-promoting attributes primarily by acting as a co-receptor for basic fibroblast growth factor (FGF-2). Suppression of perlecan causes substantial inhibition of neoplastic growth and neovascularization. Thus, perlecan is a potent inducer of neoplasm growth and angiogenesis in vivo and therapeutic interventions targeting this key modulator of tumor progression may improve neoplastic treatment.
Description:
This MAb specifically precipitates heterogeneous material of high MW, identified as perlecan, a major heparan-sulfate proteoglycan (HSPG) within all basement membranes and cell surfaces. It does not cross-react with laminin, fibronectin, or dermatran sulfate proteoglycan. Because of perlecan s strategic location and ability to store and protect growth factors, it has been strongly implicated in the control of tumor cell growth and metastatic behavior. Perlecan possesses angiogenic and growth-promoting attributes primarily by acting as a co-receptor for basic fibroblast growth factor (FGF-2). Suppression of perlecan causes substantial inhibition of neoplastic growth and neovascularization. Thus, perlecan is a potent inducer of neoplasm growth and angiogenesis in vivo and therapeutic interventions targeting this key modulator of tumor progression may improve neoplastic treatment.
Description:
Reacts with human CD59, a 20 kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). This MAb is useful for study on GPI-anchored proteins, PNH and CD59 functions. CD59 is widely distributed on cells in all tissues. The expression of CD59 on erythrocytes is important for their survival.
Description:
This antibody reacts with human CD59, a 20 kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. CD59 is widely distributed on cells in all tissues. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. The expression of CD59 on erythrocytes is important for their survival. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). It is useful for study on GPI-anchored proteins, PNH and CD59 functions.
Description:
Reacts with human CD59, a 20 kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). This MAb is useful for study on GPI-anchored proteins, PNH and CD59 functions. CD59 is widely distributed on cells in all tissues. The expression of CD59 on erythrocytes is important for their survival.
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