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Indium(III)+phosphate
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Indium(III)+phosphate
Catalog Number:
(10401-112)
Supplier:
Bioss
Description:
Defects in G6PD are the cause of chronic non-spherocytic hemolytic anemia (CNSHA) . Deficiency of G6PD is associated with hemolytic anemia in two different situations. First, in areas in which malaria has been endemic, G6PD-deficiency alleles have reached high frequencies (1% to 50%) and deficient individuals, though essentially asymptomatic in the steady state, have a high risk of acute hemolytic attacks. Secondly, sporadic cases of G6PD deficiency occur at a very low frequencies, and they usually present a more severe phenotype. Several types of CNSHA are recognized. Class-I variants are associated with severe NSHA; class-II have an activity <10% of normal; class-III have an activity of 10% to 60% of normal; class-IV have near normal activity.
Catalog Number:
(102995-710)
Supplier:
Cell Sciences
Description:
Flow Cytometry: Use 10 µl to label 1x10E6 cells or 100 µl of whole blood.
Catalog Number:
(75844-198)
Supplier:
BIOGEMS INTERNATIONAL INC.
Description:
The 2.4G2 monoclonal antibody specifically reacts with an epitope on the extracellular domain of the mouse CD16 (Fc γ III) and CD 32 (Fc γ II). CD16 and CD32 are low affinity receptors for the IgG Fc domain and are expressed by B lymphocytes, NK cells, kupffer cells, mast cells, monocytes, macrophages, granulocytes, immature thymocytes, neutrophils, and some activated mature T cells.The 2.4G2 antibody blocks the binding of immunoglobulins to CD16 and CD32, and possibly to Fc γ I receptor.
Catalog Number:
(75842-964)
Supplier:
BIOGEMS INTERNATIONAL INC.
Description:
The 2.4G2 monoclonal antibody specifically reacts with an epitope on the extracellular domain of the mouse CD16 (Fc γ III) and CD 32 (Fc γ II). CD16 and CD32 are low affinity receptors for the IgG Fc domain and are expressed by B lymphocytes, NK cells, kupffer cells, mast cells, monocytes, macrophages, granulocytes, immature thymocytes, neutrophils, and some activated mature T cells.The 2.4G2 antibody blocks the binding of immunoglobulins to CD16 and CD32, and possibly to Fc γ I receptor.
Catalog Number:
(10405-232)
Supplier:
Bioss
Description:
Defects in G6PD are the cause of chronic non-spherocytic hemolytic anemia (CNSHA) . Deficiency of G6PD is associated with hemolytic anemia in two different situations. First, in areas in which malaria has been endemic, G6PD-deficiency alleles have reached high frequencies (1% to 50%) and deficient individuals, though essentially asymptomatic in the steady state, have a high risk of acute hemolytic attacks. Secondly, sporadic cases of G6PD deficiency occur at a very low frequencies, and they usually present a more severe phenotype. Several types of CNSHA are recognized. Class-I variants are associated with severe NSHA; class-II have an activity <10% of normal; class-III have an activity of 10% to 60% of normal; class-IV have near normal activity.
Catalog Number:
(75842-968)
Supplier:
BIOGEMS INTERNATIONAL INC.
Description:
The 2.4G2 monoclonal antibody specifically reacts with an epitope on the extracellular domain of the mouse CD16 (Fc γ III) and CD 32 (Fc γ II). CD16 and CD32 are low affinity receptors for the IgG Fc domain and are expressed by B lymphocytes, NK cells, kupffer cells, mast cells, monocytes, macrophages, granulocytes, immature thymocytes, neutrophils, and some activated mature T cells.The 2.4G2 antibody blocks the binding of immunoglobulins to CD16 and CD32, and possibly to Fc γ I receptor.
Catalog Number:
(75842-966)
Supplier:
BIOGEMS INTERNATIONAL INC.
Description:
The 2.4G2 monoclonal antibody specifically reacts with an epitope on the extracellular domain of the mouse CD16 (Fc γ III) and CD 32 (Fc γ II). CD16 and CD32 are low affinity receptors for the IgG Fc domain and are expressed by B lymphocytes, NK cells, kupffer cells, mast cells, monocytes, macrophages, granulocytes, immature thymocytes, neutrophils, and some activated mature T cells.The 2.4G2 antibody blocks the binding of immunoglobulins to CD16 and CD32, and possibly to Fc γ I receptor.
Catalog Number:
(10401-118)
Supplier:
Bioss
Description:
Defects in G6PD are the cause of chronic non-spherocytic hemolytic anemia (CNSHA) . Deficiency of G6PD is associated with hemolytic anemia in two different situations. First, in areas in which malaria has been endemic, G6PD-deficiency alleles have reached high frequencies (1% to 50%) and deficient individuals, though essentially asymptomatic in the steady state, have a high risk of acute hemolytic attacks. Secondly, sporadic cases of G6PD deficiency occur at a very low frequencies, and they usually present a more severe phenotype. Several types of CNSHA are recognized. Class-I variants are associated with severe NSHA; class-II have an activity <10% of normal; class-III have an activity of 10% to 60% of normal; class-IV have near normal activity.
Catalog Number:
(10405-230)
Supplier:
Bioss
Description:
Defects in G6PD are the cause of chronic non-spherocytic hemolytic anemia (CNSHA) . Deficiency of G6PD is associated with hemolytic anemia in two different situations. First, in areas in which malaria has been endemic, G6PD-deficiency alleles have reached high frequencies (1% to 50%) and deficient individuals, though essentially asymptomatic in the steady state, have a high risk of acute hemolytic attacks. Secondly, sporadic cases of G6PD deficiency occur at a very low frequencies, and they usually present a more severe phenotype. Several types of CNSHA are recognized. Class-I variants are associated with severe NSHA; class-II have an activity <10% of normal; class-III have an activity of 10% to 60% of normal; class-IV have near normal activity.
Catalog Number:
(10406-090)
Supplier:
Bioss
Description:
Defects in G6PD are the cause of chronic non-spherocytic hemolytic anemia (CNSHA) . Deficiency of G6PD is associated with hemolytic anemia in two different situations. First, in areas in which malaria has been endemic, G6PD-deficiency alleles have reached high frequencies (1% to 50%) and deficient individuals, though essentially asymptomatic in the steady state, have a high risk of acute hemolytic attacks. Secondly, sporadic cases of G6PD deficiency occur at a very low frequencies, and they usually present a more severe phenotype. Several types of CNSHA are recognized. Class-I variants are associated with severe NSHA; class-II have an activity <10% of normal; class-III have an activity of 10% to 60% of normal; class-IV have near normal activity.
Catalog Number:
(10401-116)
Supplier:
Bioss
Description:
Defects in G6PD are the cause of chronic non-spherocytic hemolytic anemia (CNSHA) . Deficiency of G6PD is associated with hemolytic anemia in two different situations. First, in areas in which malaria has been endemic, G6PD-deficiency alleles have reached high frequencies (1% to 50%) and deficient individuals, though essentially asymptomatic in the steady state, have a high risk of acute hemolytic attacks. Secondly, sporadic cases of G6PD deficiency occur at a very low frequencies, and they usually present a more severe phenotype. Several types of CNSHA are recognized. Class-I variants are associated with severe NSHA; class-II have an activity <10% of normal; class-III have an activity of 10% to 60% of normal; class-IV have near normal activity.
Catalog Number:
(10250-776)
Supplier:
Bioss
Description:
Myotubularin-related protein 14 (MTMR14), also known as Jumpy, is a myotubularin-related phosphoinositol-3-phosphate (PI3P) phosphatase (1). Mutations in the MTMR14 gene have been associated with centronuclear myopathy (1). MTMR14 deficiency in mice leads to altered calcium homeostasis and muscle disorders (2). MTMR14 has also been shown to play a role in autophagy, a process that is highly regulated by phosphatidylinositides through the type III PI3K, Vps34 (3). MTMR14 was localized to autophagic isolation membranes and early autophagosomes (3). In these studies, MTMR14 inhibited autophagy and mutations of MTMR14 associated with centronuclear myopathy were also defective in autophagy inhibition. In zebrafish, MTMR14 knockdown was shown to increase the number of autophagosomes, suggesting that its activity is associated with an inhibition of autophagy (4).
Catalog Number:
(10251-540)
Supplier:
Bioss
Description:
Myotubularin-related protein 14 (MTMR14), also known as Jumpy, is a myotubularin-related phosphoinositol-3-phosphate (PI3P) phosphatase (1). Mutations in the MTMR14 gene have been associated with centronuclear myopathy (1). MTMR14 deficiency in mice leads to altered calcium homeostasis and muscle disorders (2). MTMR14 has also been shown to play a role in autophagy, a process that is highly regulated by phosphatidylinositides through the type III PI3K, Vps34 (3). MTMR14 was localized to autophagic isolation membranes and early autophagosomes (3). In these studies, MTMR14 inhibited autophagy and mutations of MTMR14 associated with centronuclear myopathy were also defective in autophagy inhibition. In zebrafish, MTMR14 knockdown was shown to increase the number of autophagosomes, suggesting that its activity is associated with an inhibition of autophagy (4).
Catalog Number:
(10251-544)
Supplier:
Bioss
Description:
Myotubularin-related protein 14 (MTMR14), also known as Jumpy, is a myotubularin-related phosphoinositol-3-phosphate (PI3P) phosphatase (1). Mutations in the MTMR14 gene have been associated with centronuclear myopathy (1). MTMR14 deficiency in mice leads to altered calcium homeostasis and muscle disorders (2). MTMR14 has also been shown to play a role in autophagy, a process that is highly regulated by phosphatidylinositides through the type III PI3K, Vps34 (3). MTMR14 was localized to autophagic isolation membranes and early autophagosomes (3). In these studies, MTMR14 inhibited autophagy and mutations of MTMR14 associated with centronuclear myopathy were also defective in autophagy inhibition. In zebrafish, MTMR14 knockdown was shown to increase the number of autophagosomes, suggesting that its activity is associated with an inhibition of autophagy (4).
Catalog Number:
(10251-590)
Supplier:
Bioss
Description:
Myotubularin-related protein 14 (MTMR14), also known as Jumpy, is a myotubularin-related phosphoinositol-3-phosphate (PI3P) phosphatase (1). Mutations in the MTMR14 gene have been associated with centronuclear myopathy (1). MTMR14 deficiency in mice leads to altered calcium homeostasis and muscle disorders (2). MTMR14 has also been shown to play a role in autophagy, a process that is highly regulated by phosphatidylinositides through the type III PI3K, Vps34 (3). MTMR14 was localized to autophagic isolation membranes and early autophagosomes (3). In these studies, MTMR14 inhibited autophagy and mutations of MTMR14 associated with centronuclear myopathy were also defective in autophagy inhibition. In zebrafish, MTMR14 knockdown was shown to increase the number of autophagosomes, suggesting that its activity is associated with an inhibition of autophagy (4).
Catalog Number:
(75929-638)
Supplier:
Rockland Immunochemical
Description:
The lysosomal integral membrane protein 2 (LIMP2) is a heavily glycosylated type III transmembrane protein, the majority of which exists in the lumen of the lysosome and a cytoplasmic domain of approximately 20 amino acids. A deficiency of LIMP2 in mice causes uretic pelvic junction obstruction, deafness, and peripheral neuropathy associated with impaired vesicular trafficking and distribution of apically expressed proteins. More recently, LIMP2 was shown to act as a receptor to bind beta-glucocerebrosidase, the enzyme defective in Gaucher disease, a lysosomal storage disorder. LIMP2-deficient mice showed missorted as well as secreted beta-glucocerebrosidase, suggesting that LIMP2 also functions as the mannose-6-phosphate-independent trafficking receptor.
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 is still displayed and you need assistance, please call us at 1-800-932-5000.
Stock for this item is limited, but may be available in a warehouse close to you. Please make sure that you are logged in to the site so that available stock can be displayed. If the
is still displayed and you need assistance, please call us at 1-800-932-5000.
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