11-0419-41

antibody from Invitrogen Antibodies

Targeting: ITGA2B CD41, CD41B, GP2B, PPP1R93

Provider product page for 11-0419-41

Flow cytometry

Other assay

Antibody data

Antibody Data
Antigen structure
References [16]
Comments [0]
Validations
Flow cytometry [1]
Other assay [4]

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Product number: 11-0419-41 - Provider product page
Provider: Invitrogen Antibodies
Product name: CD41a Monoclonal Antibody (HIP8), FITC, eBioscience™
Antibody type: Monoclonal
Antigen: Other
Description: Description: The HIP8 monoclonal antibody reacts with the human CD41 molecule, the integrin alphaIIb also known as platelet GPIIb. CD41 non-covalently associates with integrin beta3 (GPIIIa, CD61) and is expressed by megakaryocytes and platelets. The CD41/CD61 complex is a receptor for fibronectin, fibrinogen, von Willebrand factor, vitronectin and thrombospondin and mediates platelets aggregation. HIP8 blocks platelet aggregation.
Conjugate: Green dye
Antibody clone number: HIP8
Concentration: 5 µL/Test

ITGA2B protein structure - 11-0419-41 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure A2 Platelets bound to T cells upon activation in coculture. CD4 + CD25 - T cells were cocultured with or without platelets at the ratio of 1:50 and stimulated with 0.5 ug/mL anti-CD3 mAb and 1.0 ug/mL anti-CD28 mAb for 6 days. At day 1 and 6, platelet-T cell conjugates (CD41a + CD4 + double-positive cells) were analyzed via flow cytometry. For assessment of GARP expression, only CD4 + CD41a- cells were included in the analysis (indicated by the pregating on the upper left (UL)). GARP expression was normalized to the untreated (w/o) control. Dot plots show one representative result of five independent experiments. Isotype controls are shown ( n = 5, box and whiskers, medians + min/max, ** p
Conjugate: Green dye

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 3 Ovarian cancer ascites induces rapid platelet activation and aggregation that is partially abrogated by DNase and protease treatments. a - g Ascites were collected from patients with newly diagnosed advanced EOC and 500 g supernatants (ASC) were used. a Floating aggregates were collected from ascites before centrifugation and analysed by H&E. Abundant neutrophils (black box) and a sparse number of tumour cells (black arrow) embedded in fibrin deposits (pink filaments) were identified. b , c CD41 + PMP were measured in ascites supernatants by modified flow cytometry ( n = 2). Variability exists between different patients (B, left) 16.58% and (C, left) 1.16% CD41a + . In parallel, samples were 0.1 um-filtered to remove microparticles as a specificity control ( b , c , right panels). d - g . Platelets were isolated from peripheral blood of healthy donors and murine cardiac puncture. d Donor platelets were exposed to Tyrode's buffer with 1 mM CaCl 2 (negative control) or ascites supernatants ( n = 7) in the presence of 1 mM CaCl 2 for 30 minutes prior to staining for flow cytometry. Representative density plots show increased number of P-selectin + platelets (P11 gate) after exposure to ascites supernatants, which is quantified to the right (**, p < 0.01 ). E) Naive murine platelets were exposed to the same ascites supernatants ( n = 7), resulting in increased P-selectin expression and loss of CD42d from the surface of platelets within 15 minutes. The proportion of platele
Conjugate: Green dye

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 1 Characterization of human blood from influenza-infected patients. a - d Blood from influenza-infected patients was fixed after intravenous collection and stained as described in Methods. In all cases DNA was assessed by DAPI. a Many platelets appeared similar to those observed in control blood from healthy donors with a size of 2-5 um. b Some platelets from influenza-infected patients had undergone spreading with a distinctive distribution of CD41. c Platelets and platelet microparticles associated with DNA (arrow). d Spread platelets were found surrounding released DNA with distinct DNA content in their center. Of note, blood from influenza-infected patients and controls in ( a - d ) was not permeabilized. Since formaldehyde can cause certain levels of permeabilization as a function of cross-linking positive staining in control samples for H4 and MPO do not necessarily indicate activation. e - g Levels of proteins related to DNA release in the plasma of influenza-infected patients assessed by ELISA. Source data are provided as a Source Data file. e neutrophil elastase, f myeloperoxidase (MPO), and g histone nucleosome core. The graphs represent the average +- SD of healthy donors ( n = 15) and influenza-infected patients ( n = 18); significance for ( e - g ) was assessed by Mann-Whitney U test, star symbol (*) indicates p < 0.0001. h , i To synchronize time of influenza presence as a function of infection and quantify the released DNA, we
Conjugate: Green dye

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 1. Expression of ACE2 and TMPRSS2 in Platelets by Confocal Microscopy. Platelets isolated from venous blood of healthy individuals was stained for 1h with the following antibodies: CD41 (platelet-specific marker), ACE2, TMPRSS2, and DAPI to eliminate any DNA components. Mounted slides were resolved by confocal fluorescent microscopy using a 100x objective lens. Images are representative of n=6 donors for ACE2 and n=3 for TMPRSS2. Each image represents a different donor. The scale bar is noted.
Conjugate: Green dye