anti-Abciximab antibody Anti-drug antibodies (ADAs) generated in subjects following administration of Abciximab.
Abciximab Abciximab biologic drug binds Homo sapiens ITGA2B,Homo sapiens ITGB3
Homo sapiens ITGB3 Integrin beta-3
Protein names Integrin beta-3
Gene names ITGB3
Protein family Belongs to the integrin beta chain family
Function (Microbial infection) In case of HIV-1 infection, the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi's sarcoma lesions
Structure (Microbial infection) Interacts with HIV-1 Tat (PubMed:10397733). ITGAV:ITGB3 interacts with AGRA2 (PubMed:16982628)
Post-translational modification Phosphorylated on tyrosine residues in response to thrombin-induced platelet aggregation. Probably involved in outside-in signaling. A peptide (AA 740-762) is capable of binding GRB2 only when both Tyr-773 and Tyr-785 are phosphorylated. Phosphorylation of Thr-779 inhibits SHC binding
Involvement in disease Fetomaternal alloimmune thrombocytopenia 1 A form of fetomaternal alloimmune thrombocytopenia, a bleeding disorder caused by maternal/fetal incompatibility for platelet alloantigens and arising when a fetus inherits a paternal platelet alloantigen that the mother does not possess. During pregnancy, as well as parturition, maternal alloantibodies against paternally-inherited platelet antigens cause destruction of fetal platelets and fetal/neonatal thrombocytopenia. Disease severity and clinical features in the fetus or neonate are heterogeneous. While most fetuses remain asymptomatic, others develop skin bleedings (petechiae) or internal organ bleedings. The most severe symptom is intracranial hemorrhage that is mostly discovered postnatally and can result in neurological complications or even death. Mothers with circulating platelet alloantibodies may experience miscarriage. FMAIT1 transmission pattern is consistent with autosomal dominant paternal inheritance.
Glanzmann thrombasthenia 2 A form of Glanzmann thrombasthenia, a disorder characterized by failure of platelet aggregation, absent or diminished clot retraction, and mucocutaneous bleeding of mild-to-moderate severity. Glanzmann thrombasthenia has been classified into clinical types I and II. In type I, platelets show absence of glycoprotein IIb-IIIa complexes at their surface and lack fibrinogen and clot retraction capability. In type II, the platelets express glycoprotein IIb-IIIa complexes at reduced levels, have detectable amounts of fibrinogen, and have low or moderate clot retraction capability.
Bleeding disorder, platelet-type, 24 An autosomal dominant disorder of platelet production characterized by congenital macrothrombocytopenia and platelet anisocytosis. Affected individuals may have no or only mildly increased bleeding tendency.
Already shown entity_id 167; skipped to avoid loop.
Homo sapiens ITGA2B Integrin alpha-IIb
Protein names Integrin alpha-IIb
Gene names ITGA2B
Protein family Belongs to the integrin alpha chain family
Function Integrin alpha-IIb/beta-3 (ITGA2B:ITGB3) is a receptor for fibronectin, fibrinogen, plasminogen, prothrombin, thrombospondin and vitronectin. It recognizes the sequence R-G-D in a wide array of ligands. It recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain (By similarity). Following activation integrin alpha-IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen (PubMed:9111081). This step leads to rapid platelet aggregation which physically plugs ruptured endothelial cell surface (By similarity). Integrin ITGA2B:ITGB3 is also the receptor of erythrocyte-specific ICAM4 ligand involved in heterotypic cell-cell adhesion between erythrocytes and activated platelets (PubMed:12477717)
Subcellular location Cell membrane
Structure Heterodimer of an alpha and a beta subunit. The alpha subunit is composed of a heavy and a light chain linked by a disulfide bond. Alpha-IIb associates with beta-3. Directly interacts with RNF181. Interacts (via C-terminus cytoplasmic tail region) with CIB1; the interaction is direct and calcium-dependent. Interacts (via C-terminus cytoplasmic tail region) with CIB2, CIB3 and CIB4; the interactions are stabilized/increased in a calcium and magnesium-dependent manner. ITGA2B:ITGB3 interacts with PPIA/CYPA; the interaction is ROS and PPIase activity-dependent and is increased in the presence of thrombin (By similarity). ITGA2B:ITGB3 interacts with SELP (via C-type lectin domain); the interaction mediates cell-cell interaction and adhesion (PubMed:37184585)
Post-translational modification Cleaved by ELANE; the cleavage promotes activation of platelet fibrinogen receptor integrin alpha-IIb/beta-3
Involvement in disease Fetomaternal alloimmune thrombocytopenia 2 A form of fetomaternal alloimmune thrombocytopenia, a bleeding disorder caused by maternal/fetal incompatibility for platelet alloantigens and arising when a fetus inherits a paternal platelet alloantigen that the mother does not possess. During pregnancy, as well as parturition, maternal alloantibodies against paternally-inherited platelet antigens cause destruction of fetal platelets and fetal/neonatal thrombocytopenia. Disease severity and clinical features in the fetus or neonate are heterogeneous. While most fetuses remain asymptomatic, others develop skin bleedings (petechiae) or internal organ bleedings. The most severe symptom is intracranial hemorrhage that is mostly discovered postnatally and can result in neurological complications or even death. Mothers with circulating platelet alloantibodies may experience miscarriage. FMAIT2 transmission pattern is consistent with autosomal dominant paternal inheritance.
Glanzmann thrombasthenia 1 A form of Glanzmann thrombasthenia, a disorder characterized by failure of platelet aggregation, absent or diminished clot retraction, and mucocutaneous bleeding of mild-to-moderate severity. Glanzmann thrombasthenia has been classified into clinical types I and II. In type I, platelets show absence of glycoprotein IIb-IIIa complexes at their surface and lack fibrinogen and clot retraction capability. In type II, the platelets express glycoprotein IIb-IIIa complexes at reduced levels, have detectable amounts of fibrinogen, and have low or moderate clot retraction capability. GT1 inheritance is autosomal recessive.
Bleeding disorder, platelet-type, 16 An autosomal dominant form of congenital macrothrombocytopenia associated with platelet anisocytosis. It is a disorder of platelet production. Affected individuals may have no or only mildly increased bleeding tendency. In vitro studies show mild platelet functional abnormalities.
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Homo sapiens LFA-1 ITGB2 (CD18) + ITGAL (CD11a) integrin heterodimer
Already shown entity_id 167; skipped to avoid loop.
Homo sapiens ITGA2 Integrin alpha-2
Protein names Integrin alpha-2
Gene names ITGA2
Protein family Belongs to the integrin alpha chain family
Function (Microbial infection) Integrin ITGA2:ITGB1 acts as a receptor for Human echoviruses 1 and 8
Subcellular location Membrane
Structure (Microbial infection) Integrin ITGA2:ITGB1 interacts with human echoviruses 1 and 8 capsid proteins
Involvement in disease Fetomaternal alloimmune thrombocytopenia 3 A form of fetomaternal alloimmune thrombocytopenia, a bleeding disorder caused by maternal/fetal incompatibility for platelet alloantigens and arising when a fetus inherits a paternal platelet alloantigen that the mother does not possess. During pregnancy, as well as parturition, maternal alloantibodies against paternally-inherited platelet antigens cause destruction of fetal platelets and fetal/neonatal thrombocytopenia. Disease severity and clinical features in the fetus or neonate are heterogeneous. While most fetuses remain asymptomatic, others develop skin bleedings (petechiae) or internal organ bleedings. The most severe symptom is intracranial hemorrhage that is mostly discovered postnatally and can result in neurological complications or even death. Mothers with circulating platelet alloantibodies may experience miscarriage. FMAIT3 transmission pattern is consistent with autosomal dominant paternal inheritance.
Already shown entity_id 835; skipped to avoid loop.
Homo sapiens CR4 ITGB2 (CD18) + ITGAX (CD11c) integrin heterodimer
Already shown entity_id 167; skipped to avoid loop.
Homo sapiens ITGAV Integrin alpha-V
Protein names Integrin alpha-V
Gene names ITGAV
Protein family Belongs to the integrin alpha chain family
Function (Microbial infection) In case of HIV-1 infection, the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi's sarcoma lesions
Already shown entity_id 837; skipped to avoid loop.
Homo sapiens ITGA2B Integrin alpha-IIb
Protein names Integrin alpha-IIb
Gene names ITGA2B
Protein family Belongs to the integrin alpha chain family
Function Integrin alpha-IIb/beta-3 (ITGA2B:ITGB3) is a receptor for fibronectin, fibrinogen, plasminogen, prothrombin, thrombospondin and vitronectin. It recognizes the sequence R-G-D in a wide array of ligands. It recognizes the sequence H-H-L-G-G-G-A-K-Q-A-G-D-V in fibrinogen gamma chain (By similarity). Following activation integrin alpha-IIb/beta-3 brings about platelet/platelet interaction through binding of soluble fibrinogen (PubMed:9111081). This step leads to rapid platelet aggregation which physically plugs ruptured endothelial cell surface (By similarity). Integrin ITGA2B:ITGB3 is also the receptor of erythrocyte-specific ICAM4 ligand involved in heterotypic cell-cell adhesion between erythrocytes and activated platelets (PubMed:12477717)
Subcellular location Cell membrane
Structure Heterodimer of an alpha and a beta subunit. The alpha subunit is composed of a heavy and a light chain linked by a disulfide bond. Alpha-IIb associates with beta-3. Directly interacts with RNF181. Interacts (via C-terminus cytoplasmic tail region) with CIB1; the interaction is direct and calcium-dependent. Interacts (via C-terminus cytoplasmic tail region) with CIB2, CIB3 and CIB4; the interactions are stabilized/increased in a calcium and magnesium-dependent manner. ITGA2B:ITGB3 interacts with PPIA/CYPA; the interaction is ROS and PPIase activity-dependent and is increased in the presence of thrombin (By similarity). ITGA2B:ITGB3 interacts with SELP (via C-type lectin domain); the interaction mediates cell-cell interaction and adhesion (PubMed:37184585)
Post-translational modification Cleaved by ELANE; the cleavage promotes activation of platelet fibrinogen receptor integrin alpha-IIb/beta-3
Involvement in disease Fetomaternal alloimmune thrombocytopenia 2 A form of fetomaternal alloimmune thrombocytopenia, a bleeding disorder caused by maternal/fetal incompatibility for platelet alloantigens and arising when a fetus inherits a paternal platelet alloantigen that the mother does not possess. During pregnancy, as well as parturition, maternal alloantibodies against paternally-inherited platelet antigens cause destruction of fetal platelets and fetal/neonatal thrombocytopenia. Disease severity and clinical features in the fetus or neonate are heterogeneous. While most fetuses remain asymptomatic, others develop skin bleedings (petechiae) or internal organ bleedings. The most severe symptom is intracranial hemorrhage that is mostly discovered postnatally and can result in neurological complications or even death. Mothers with circulating platelet alloantibodies may experience miscarriage. FMAIT2 transmission pattern is consistent with autosomal dominant paternal inheritance.
Glanzmann thrombasthenia 1 A form of Glanzmann thrombasthenia, a disorder characterized by failure of platelet aggregation, absent or diminished clot retraction, and mucocutaneous bleeding of mild-to-moderate severity. Glanzmann thrombasthenia has been classified into clinical types I and II. In type I, platelets show absence of glycoprotein IIb-IIIa complexes at their surface and lack fibrinogen and clot retraction capability. In type II, the platelets express glycoprotein IIb-IIIa complexes at reduced levels, have detectable amounts of fibrinogen, and have low or moderate clot retraction capability. GT1 inheritance is autosomal recessive.
Bleeding disorder, platelet-type, 16 An autosomal dominant form of congenital macrothrombocytopenia associated with platelet anisocytosis. It is a disorder of platelet production. Affected individuals may have no or only mildly increased bleeding tendency. In vitro studies show mild platelet functional abnormalities.
Protein family Belongs to the integrin beta chain family
Function (Microbial infection) In case of HIV-1 infection, the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi's sarcoma lesions
Structure (Microbial infection) Interacts with HIV-1 Tat (PubMed:10397733). ITGAV:ITGB3 interacts with AGRA2 (PubMed:16982628)
Post-translational modification Phosphorylated on tyrosine residues in response to thrombin-induced platelet aggregation. Probably involved in outside-in signaling. A peptide (AA 740-762) is capable of binding GRB2 only when both Tyr-773 and Tyr-785 are phosphorylated. Phosphorylation of Thr-779 inhibits SHC binding
Involvement in disease Fetomaternal alloimmune thrombocytopenia 1 A form of fetomaternal alloimmune thrombocytopenia, a bleeding disorder caused by maternal/fetal incompatibility for platelet alloantigens and arising when a fetus inherits a paternal platelet alloantigen that the mother does not possess. During pregnancy, as well as parturition, maternal alloantibodies against paternally-inherited platelet antigens cause destruction of fetal platelets and fetal/neonatal thrombocytopenia. Disease severity and clinical features in the fetus or neonate are heterogeneous. While most fetuses remain asymptomatic, others develop skin bleedings (petechiae) or internal organ bleedings. The most severe symptom is intracranial hemorrhage that is mostly discovered postnatally and can result in neurological complications or even death. Mothers with circulating platelet alloantibodies may experience miscarriage. FMAIT1 transmission pattern is consistent with autosomal dominant paternal inheritance.
Glanzmann thrombasthenia 2 A form of Glanzmann thrombasthenia, a disorder characterized by failure of platelet aggregation, absent or diminished clot retraction, and mucocutaneous bleeding of mild-to-moderate severity. Glanzmann thrombasthenia has been classified into clinical types I and II. In type I, platelets show absence of glycoprotein IIb-IIIa complexes at their surface and lack fibrinogen and clot retraction capability. In type II, the platelets express glycoprotein IIb-IIIa complexes at reduced levels, have detectable amounts of fibrinogen, and have low or moderate clot retraction capability.
Bleeding disorder, platelet-type, 24 An autosomal dominant disorder of platelet production characterized by congenital macrothrombocytopenia and platelet anisocytosis. Affected individuals may have no or only mildly increased bleeding tendency.
Already shown entity_id 832; skipped to avoid loop.
Homo sapiens LFA-1 ITGB2 (CD18) + ITGAL (CD11a) integrin heterodimer
Already shown entity_id 167; skipped to avoid loop.
Homo sapiens ITGA2 Integrin alpha-2
Protein names Integrin alpha-2
Gene names ITGA2
Protein family Belongs to the integrin alpha chain family
Function (Microbial infection) Integrin ITGA2:ITGB1 acts as a receptor for Human echoviruses 1 and 8
Subcellular location Membrane
Structure (Microbial infection) Integrin ITGA2:ITGB1 interacts with human echoviruses 1 and 8 capsid proteins
Involvement in disease Fetomaternal alloimmune thrombocytopenia 3 A form of fetomaternal alloimmune thrombocytopenia, a bleeding disorder caused by maternal/fetal incompatibility for platelet alloantigens and arising when a fetus inherits a paternal platelet alloantigen that the mother does not possess. During pregnancy, as well as parturition, maternal alloantibodies against paternally-inherited platelet antigens cause destruction of fetal platelets and fetal/neonatal thrombocytopenia. Disease severity and clinical features in the fetus or neonate are heterogeneous. While most fetuses remain asymptomatic, others develop skin bleedings (petechiae) or internal organ bleedings. The most severe symptom is intracranial hemorrhage that is mostly discovered postnatally and can result in neurological complications or even death. Mothers with circulating platelet alloantibodies may experience miscarriage. FMAIT3 transmission pattern is consistent with autosomal dominant paternal inheritance.
Already shown entity_id 835; skipped to avoid loop.
Homo sapiens CR4 ITGB2 (CD18) + ITGAX (CD11c) integrin heterodimer
Already shown entity_id 167; skipped to avoid loop.
Homo sapiens ITGAV Integrin alpha-V
Protein names Integrin alpha-V
Gene names ITGAV
Protein family Belongs to the integrin alpha chain family
Function (Microbial infection) In case of HIV-1 infection, the interaction with extracellular viral Tat protein seems to enhance angiogenesis in Kaposi's sarcoma lesions
Already shown entity_id 837; skipped to avoid loop.
Already shown entity_id 590; skipped to avoid loop.
Data
Standard Curve
X axis: log |
Y axis: linear
Standard
STD [ng/mL]
OD1
OD2
Average OD
Corrected OD
Blank #8
0
0.1
0.11
0.11
0
Standard #7
1.56
0.14
0.15
0.15
0.04
Standard #6
3.13
0.18
0.18
0.18
0.07
Standard #5
6.25
0.21
0.22
0.22
0.11
Standard #4
12.5
0.32
0.34
0.33
0.22
Standard #3
25
0.6
0.63
0.61
0.51
Standard #2
50
1.21
1.27
1.24
1.14
Standard #1
100
2.21
2.32
2.27
2.16
Precision
Sample
n
Mean
Standard Deviation
CV (%)
Intra Sample 1
20
3.11
0.16
5.23
Intra Sample 2
20
13.99
0.66
4.69
Intra Sample 3
20
49.67
2.41
4.86
Inter Sample 1
20
3.06
0.17
5.68
Inter Sample 2
20
12.59
0.66
5.27
Inter Sample 3
20
50.86
2.69
5.29
Recovery
Matrix
Recovery Range (%)
Average (%)
Serum(n=5)
92-104
97
EDTA Plasma(n=5)
89-102
97
HeparinPlasma(n=5)
92-105
97
Stability
37°C 1 Month (%)
2–8°C 6 Months (%)
2–8°C 12 Months (%)
80
95-100
85-98
Linearity
Sample
1:2 Dilution (%)
1:4 Dilution (%)
1:8 Dilution (%)
Serum(n=5)
92-104%
85-100%
86-96%
EDTAPlasma(n=5)
88-104%
88-99%
86-93%
Heparin Plasma(n=5)
89-97%
91-98%
86-98%
FAQ & Publications
Publications
pmid
title
authors
citation
We haven't added any publications to our database yet.
Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from the PubMed database provided by the United States National Library of Medicine at the National Institutes of Health.
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