17-0567-41

antibody from Invitrogen Antibodies

Targeting: NCAM1 CD56, NCAM

Provider product page for 17-0567-41

Flow cytometry

Other assay

Antibody data

Antibody Data
Antigen structure
References [23]
Comments [0]
Validations
Flow cytometry [1]
Other assay [9]

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Product number: 17-0567-41 - Provider product page
Provider: Invitrogen Antibodies
Product name: CD56 (NCAM) Monoclonal Antibody (CMSSB), APC, eBioscience™
Antibody type: Monoclonal
Antigen: Other
Description: Description: This CMSSB monoclonal antibody reacts with human CD56, also known as Neural Cell Adhesion Molecule (NCAM). CD56 is a highly glycosylated transmembrane molecule expressed by neurons and plays a role in the homotypic adhesion of neural cells. In the hematopoietic system, CD56 is expressed on NK cells and a subset of T cells referred to as NKT cells. Staining with CMSSB does not block binding of MEM188 or CB56. Applications Reported: This CMSSB antibody has been reported for use in flow cytometric analysis. Applications Tested: This CMSSB antibody has been pre-titrated and tested by flow cytometric analysis of normal human peripheral blood cells. This can be used at 5 µL (0.125 µg) per test. A test is defined as the amount (µg) of antibody that will stain a cell sample in a final volume of 100 µL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. Excitation: 633-647 nm; Emission: 660 nm; Laser: Red Laser. Filtration: 0.2 µm post-manufacturing filtered.
Reactivity: Human
Host: Mouse
Isotype: IgG
Antibody clone number: CMSSB
Vial size: 25 Tests
Concentration: 5 µL/Test
Storage: 4° C, store in dark, DO NOT FREEZE!

NCAM1 protein structure - 17-0567-41 shown in red.

Supportive validation

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

Supportive validation

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

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 6 Killing of hepatitis C virus subgenomic replicon cells requires interaction of innate immune cells. (A) Huh-7 Con1 cells were co-cultured with peripheral blood mononuclear cells (PBMCs), purified immune cells [natural killer (NK), plasmacytoid dendritic cells (pDC), or Monocytes (Mono)] or with a recombination of purified NK cells, pDCs and monocytes (NK + pDC + Mono) overnight. Supernatants were collected and measured for lactate dehydrogenase (LDH) activity ( n = 3). (B) Huh-7 Con1 cells were co-cultured with PBMCs, PBMCs depleted from NK cells (-NK), from pDCs (-pDC), from monocytes (-Mono), or from NK cells and pDCs (-NK -pDC) overnight. Supernatants were collected and measured for LDH activity ( n = 4). (C) Huh-7 cells were co-cultured with PBMCs overnight. NK cell (CD56 + , CD3 - ) expression of CD69, CD25, and TRAIL was analyzed by flow cytometry ( n = 4). (D-F) Huh-7 Con1 cells were co-cultured with PBMCs in the presence of an anti-TRAIL antibody or an IgG control antibody (each 10 ug/ml) overnight. LDH release was measured in the supernatant (D) , percentage of CFSE + monocytes (E) , and carboxyfluorescein succinimidyl ester (CFSE) mean fluorescence intensity (MFI) of monocytes (F) was determined ( n = 4).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1 Characterization of trophoblast-derived EVs (T-EVs). EVs were isolated from the villi according to a standard isolation procedure. A. Representative electron micrograph of T-EVs from patients with a normal pregnancy (NP), RSA patients who had an abnormal embryo karyotype (AK-RSA) and URSA patients. B. Nanoparticle tracking analysis (NTA) of T-EVs from NP, AK-RSA and URSA patients. C. A total of 30 mug of T-EVs and total villus lysates were immunoblotted with the indicated antibodies. D. After adsorption onto latex beads, T-EVs from NP, AK-RSA and URSA patients were phenotyped and analyzed by FCM with the indicated antibodies. E. After adsorption onto latex beads, T-EVs from NP, AK-RSA and URSA patients were analyzed by FCM with an anti-HLA-E PE-conjugated mAb (gray: isotype control; red: NP; green: AK-RSA; blue: URSA). F. The percentage of HLA-E + beads was statistically analyzed (n=25 in the NP group; n=13 in the AK-RSA patient group; n=12 in the URSA patient group). G. The expression of HLA-E in villus tissues from NP, AK-RSA and URSA patients was detected by an immunofluorescence assay. H. Human villus trophoblast cells, JEG-3 cells and HTR-8/Svneo cells were analyzed by FCM with an anti-HLA-E PE-conjugated mAb. Red: isotype control; blue: stained before permeabilization with IC fixation buffer (Invitrogen); green: stained after permeabilization with IC fixation buffer (Invitrogen). The data are representative of three independent experiments.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Lenvatinib insignificantly affects the immune microenvironment in NPC in humanized NSG mice. A Schematic diagram of the establishment of humanized NSG mice. B Representative FACS analysis of human CD45 + cells in mouse peripheral blood. Human CD45 + cell percentage greater than 25% was considered successful in modeling. C - E Tumor growth ( C ), tumor weights ( D ) were measured in vehicle-, anti-VEGF-, and lenvatinib-treated NPC tumors. The tumor inhibition ratio were calculated ( E ) ( n = 3 samples per group). F Representative micrographs of Ki67 + proliferative cells and cleaved caspase-3 + apoptotic cells in vehicle-, anti-VEGF-, and lenvatinib-treated NPC tumors. Scale bar = 50 mum. Quantification of Ki67 + , cleaved caspase-3 + signals, and PA index in vehicle-, anti-VEGF-, and lenvatinib-treated NPC tumors. ( n = 8 random fields per group) G Representative micrographs of CD31 + microvessels and CA9 + hypoxic areas in vehicle-, anti-VEGF-, and lenvatinib-treated NPC tumors. Scale bar in upper panel = 100 mum, scale bar in lower panel = 50 mum. Quantification of CD31 + tumor vessel parameters and CA9 + signals in vehicle-, anti-VEGF-, and lenvatinib-treated NPC tumors ( n = 8 random fields per group). H Quantification of hCD45 + hCD14 + population, hCD45 + hCD19 + population, hCD45 + hCD3 + population, and hCD45 + hCD56 + population in the NPC TME ( n = 3 samples per group). I Quantification of mCD45 + mCD11b + mF4/80 + population, mCD45 + mB220 + population, mCD45 + mC

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig. 4 SPINK1 promotes EMT, stemness and chemoresistance in prostate cancer. a Immunoblot analysis for SPINK1, E-Cadherin and Vimentin levels in stable SPINK1 -silenced (shSPINK1-1 and shSPINK1-2) and control (shSCRM) 22RV1 cells. b Biological pathways downregulated in 22RV1-shSPINK1 cells relative to 22RV1-shSCRM cells obtained by DAVID analysis. Bars represent -log 10 ( P -values). c Representative phase contrast microscopic images for the prostatospheres using same cells as a (left). Bar plots depict mean area and percent sphere formation efficiency of the prostatospheres (right). Scale bar represents 100 mum. d Hoechst-33342 staining for the side population analysis using same cells as a . Data was analyzed by putting blue and far-red filters, gated regions are marked in red for each panel. e QPCR data showing relative expression of SPINK1 in siRNA-mediated SPINK1 -silenced 22RV1 cells (top, left). Quantification of ALDH activity using flow cytometry using same cells. Flow cytometric graphs showing fluorescence intensity of catalyzed ALDH substrate in the presence or absence of DEAB. Marked windows indicate percentage of ALDH1 positive cell population. f Flow cytometric analysis demonstrating cell-cycle arrest in SPINK1 -silenced 22RV1 cells using propidium iodide (PI) DNA staining. g Flow cytometry analysis depicting cell apoptosis by Annexin V-PE and 7-AAD staining using same cells as e . h Transwell migration assay using stable SPINK1 overexpre

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1 Cell preparation, morphology, expression of specific CD markers, and total amounts of cytokine-induced killer (CIK) cells. ( A ) Overview of the CIK cell preparation schedule. ( B ) CIK cells were observed under a microscope on day 3, 5, 10 and 14 after induction of peripheral blood mononuclear cells (PBMCs) (magnification, x250). ( C ) At day 14 after induction, the cell phenotype (CD3+CD56+) was identified by flow cytometry. The mean percentage of CD3+CD56+ cells from the six donors was about 32% +- 5%. ( D ) CIK cell numbers were measured using a cell counter (LUNA automated cell counter) at the indicated time points. After 14 days of cell culture, the total number of CIK cells expanded by more than 24-fold. Data from three independent experiments were used for statistical analysis and * p < 0.05.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Flow cytometric analysis for pluripotent and lineage markers expressed on day 6 of differentiation in the presence of drugs. Alexa 647-APC and Alexa 488 antibodies were used to double stain cells to look for pluripotency (Oct4+/Brachury-), mesendoderm (Oct4-/Bra+, Bra+/FoxA2-), endoderm (FoxA2+) and neurectoderm (NCAM+, NCAM+/nestin+). (A) Antibody controls using RA-treated cells. (B) Lineage-specific marker analysis.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 3. Paired gRNA Screens Identify Cofactors of Neuronal Differentiation (A) Schematic representation of paired CRISPRa screens for neuronal-fate-determining TFs in human PSCs. A dual gRNA expression vector was used to co-express a neurogenic factor with the CAS-TF gRNA library. Two independent screens were performed with sgASCL1 and sgNGN3. (B) A volcano plot of significance (p value) versus fold change in gRNA abundance based on differential DESeq2 analysis between mCherry-high and unsorted cell populations for the sgNGN3 paired screen. Red data points indicate FDR < 0.001 (n = 3 biological replicates). Blue data points indicate a set of 100 scrambled non-targeting gRNAs. (C) The fold change in gRNA abundance for the sgASCL1 versus sgNGN3 paired screens for all positively enriched gRNAs across both screens. (D) Analysis of TF family type and basal expression level in PSCs () for the positive hits from both paired screens. (E) The fold change in gRNA abundance for a set of TFs predicted to have no activity individually and synergistic activity in the sgASCL1 and sgNGN3 paired screens. (F and G) Validations of TF cofactors for sgNGN3 with TUBB3-2A-mCherry (F) and sgASCL1 with NCAM staining (G). *p < 0.05 by global one-way ANOVA with Dunnett''s post hoc test comparing all groups to scrambled 1; n = 3 biological replicates; error bars represent SEM. See also Figure S5 .