14-0458-82

antibody from Invitrogen Antibodies

Targeting: PTPRC CD45, GP180, LCA, T200

Provider product page for 14-0458-82

Flow cytometry

Other assay

Antibody data

Antibody Data
Antigen structure
References [23]
Comments [0]
Validations
Flow cytometry [1]
Other assay [7]

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Product number: 14-0458-82 - Provider product page
Provider: Invitrogen Antibodies
Product name: CD45RA Monoclonal Antibody (HI100), eBioscience™
Antibody type: Monoclonal
Antigen: Other
Description: Description: The HI100 monoclonal antibody reacts with human CD45RA, a 220 kDa molecule expressed by subpopulations of CD4+ peripheral T lymphocytes, CD8+ peripheral T lymphocytes, and B cells. The CD45RA+ T cell populations are mainly naive/virgin allowing the use of HI100 mAb as a phenotypic marker to discriminate T cell subsets.
Antibody clone number: HI100
Concentration: 0.5 mg/mL

PTPRC protein structure - 14-0458-82 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 6 T cell activation marker expression is unaffected in cells processed via uVS . Flow cytometry was used to quantify the surface level expression of key T cell activation markers (CD69, CD154, CD44, CCR7, CD45RA and CD25) in T cells processed with uVS (processed cells, red dashed) compared to non-processed cells (handling control, blue solid) 24 hours post transfection. Histogram overlays represent expression levels as a percent of maximum value of each marker for a representative sample for each condition. Experiment was performed in triplicate.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 1 The distribution of CD4+ and CD8+ T cells subsets in human lung cancer. PBMCs were isolated from the blood of lung cancer patients and healthy donors and analyzed by flow cytometry. a The frequency of the CD3+CD4+ T cells and CD3+CD8+ T cells in the HD-PBMC, PBMCs from healthy donors; NSCLC-PBMC, PBMCs from non-small lung cancer patients, Normal-Ly, from healthy lymph node, NSCLC-Ly, tumor infiltrated lymph node from non-small lung cancer patients. b Representative flow cytometric analyses of CD45RA and CCR7 expression in CD3+CD4+ T cells and CD3+CD8+ T cells, indicating naive T cells (CD45RA+/CD45RO-CCR7+, top right quadrant ), terminal effector T cells (CD45RA+/CD45RO-CCR7-, bottom right quadrant ), central memory T cells (Tcm, CD45RO+/CD45RA-CCR7+, top left quadrant ), and effector memory T cells (Tem, CD45RO+/CD45RA-CCR7-, bottom left quadrant ), gated on the forward and side scatter of the lymphocyte populations. c The frequency and absolute number of the CD4+ ( top ) and CD8+ ( bottom ), Tn ( middle gray ), Teff ( black ), Tcm ( grey ), and Tem ( dark grey ) cell subsets in the blood from the non small cell lung cancer patients and healthy donors. d The events of Tn, Teff, Tcm and Tem cell subsets of CD4+ and CD8+ cells in the blood from non small cell lung cancer patients and healthy donors, expressed as the mean +- SEM. * p < 0.05; ** p < 0.005; *** p < 0.001; Mann-Whitney test (two-tailed) and non-paired Student's t-test

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1. Purity of CD3 + CD4 + CD45RA + T cells, CD3 + CD8 + T cells and CD4 + CD25 + FoxP3 + Treg cells. CD3 + CD4 + CD45RA + T cells and CD3 + CD8 + T cells were purified by magnetic cell sorting, and their purity was determined by flow cytometry. (A) The purity of CD3 + CD4 + CD45RA + T cells was 99.45% (CD3 + T cells, 99.6%; CD4 + CD45RA + T cells, 99.85%). (B) The purity of CD3 + CD8 + T cells was 95.32%. (C) The purity of CD4 + CD25 + FoxP3 + Treg cells was 93.15% (CD4 + T cells, 99.5%; CD25 + FoxP3 + T cells, 93.62%). (D) miR-155 expression in T cells of the patients with vitiligo and healthy donor was detected by reverse transcription quantitative polymerase chain reaction. **P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 1 Non-genetic adaptation drives clinical resistance in AML. a Meta-analysis from four independent studies analysing either the whole genome or whole exome of AML patients at diagnosis and relapse. Mutations are defined as non-synonymous changes within the coding sequence of any gene. Shared mutations are mutations present at both diagnosis and relapse. Whole exome sequencing data from Li et al. (REF 4 ) was analysed to access the mutations in known AML genes, as defined by the authors. b Schematic of the treatment regime and bone marrow blast percentage for patient BET001 over the clinical trial treatment course (top panel). t-SNE analysis of 7360 individual blast cells isolated from patient BET001 at baseline, remission and relapse (bottom panel). scRNA-seq and genomic DNA sampling points are highlighted on the schematic. c Schematic of treatment regime and bone marrow blast percentage for patient BET002 over the clinical trial treatment course (top panel). t-SNE analysis of 6349 single blast cells isolated from patient BET002 at baseline and relapse (bottom panel). scRNA-seq and genomic DNA sampling points are highlighted on the schematic. d Flow cytometry analysis of cells from patient BET002 at baseline and relapse identifies enrichment for LMPP-like LSCs at relapse based on CD34 + CD38-CD90-CD45RA + expression. Gating strategy is defined by boxes. e Expression analysis of selected LSC signature genes (defined in REF 15 ) in blast cells from patient BET00