Lyn ELISA Kit

Name: Lyn ELISA Kit
SKU: DEIA-XYA1145
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human; Mouse; Rat

Intended Use

The Lyn Colorimetric Cell-Based ELISA Kit allows for the qualitative detection of Lyn and the effects that certain stimulation conditions have on Lyn expression in different cell lines.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 1 Plate.
2. 10x TBS: 24 mL (10x), Clear.
3. Quenching Buffer, 24 mL (1x), Clear.
4. Blocking Buffer, 50 mL (1x), Clear.
5. 10x Wash Buffer, 50 mL (10x), Clear.
6. 100x Anti-Lyn Antibody (Rabbit Polyclonal), 60 μL (100x), Purple.
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal), 60 μL (100x), Green.
8. HRP-Conjugated Anti-Rabbit IgG Antibody, 6 mL (1x), Glass.
9. HRP-Conjugated Anti-Mouse IgG Antibody, 6 mL (1x), Glass.
10. Primary Antibody Diluent, 12 mL (1x), Clear.
11. Ready-to-Use Substrate, 12 mL (1x), Brown.
12. Stop Solution, 12 mL (1x), Clear.
13. Crystal Violet Solution, 6 mL (1x), Glass.
14. SDS Solution, 24 mL (1x), Clear.
15. Adhesive Plate Seals, 4 Seals.

Storage

4°C/6 Months

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Reticulocyte and red blood cell deformation triggers specific phosphorylation events

BLOOD ADVANCES

Authors: Moura, Pedro L.; Iragorri, Maria A. Lizarralde; Francais, Olivier; Le Pioufle, Bruno; Dobbe, Johannes G. G.; Streekstra, Geert J.; El Nemer, Wassim; Toye, Ashley M.; Satchwell, Timothy J.

Abstract

The capacity to undergo substantial deformation is a defining characteristic of the red blood cell (RBC), facilitating transit through the splenic interendothelial slits and microvasculature. Establishment of this remarkable property occurs during a process of reticulocyte maturation that begins with egress through micron-wide pores in the bone marrow and is completed within the circulation. The requirement to undertake repeated cycles of deformation necessitates that both reticulocytes and erythrocytes regulate membrane-cytoskeletal protein interactions in order to maintain cellular stability. In the absence of transcriptional activity, modulation of these interactions in RBCs is likely to be achieved primarily through specific protein posttranslational modifications, which at present remain undefined. In this study, we use high-throughput methods to define the processes that underlie the response to deformation and shear stress in both reticulocytes and erythrocytes. Through combination of a bead-based microsphiltration assay with phosphoproteomics we describe posttranslational modification of RBC proteins associated with deformation. Using microsphiltration and microfluidic biochip-based assays, we explore the effect of inhibiting kinases identified using this dataset. We demonstrate roles for GSK3 and Lyn in capillary transit and maintenance of membrane stability following deformation and show that combined inhibition of these kinases significantly decreases reticulocyte capacity to undergo repeated deformation. Finally, we derive a comprehensive and integrative phosphoproteomic dataset that provides a valuable resource for further mechanistic dissection of the molecular pathways that underlie the RBC's response to mechanical stimuli and for the study of reticulocyte maturation.

Comprehensive diagnostics of acute myeloid leukemia by whole transcriptome RNA sequencing

LEUKEMIA

Authors: Arindrarto, Wibowo; Borras, Daniel M.; de Groen, Ruben A. L.; van den Berg, Redmar R.; Locher, Irene J.; van Diessen, Saskia A. M. E.; van der Holst, Rosalie; van der Meijden, Edith D.; Honders, M. Willy; de Leeuw, Rick H.; Verlaat, Wina; Jedema, Inge; Kroes, Wilma G. M.; Knijnenburg, Jeroen; van Wezel, Tom; Vermaat, Joost S. P.; Valk, Peter J. M.; Janssen, Bart; de Knijff, Peter; van Bergen, Cornelis A. M.; van den Akker, Erik B.; 't Hoen, Peter A. C.; Kielbasa, Szymon M.; Laros, Jeroen F. J.; Griffioen, Marieke; Veelken, Hendrik

Abstract

Acute myeloid leukemia (AML) is caused by genetic aberrations that also govern the prognosis of patients and guide risk-adapted and targeted therapy. Genetic aberrations in AML are structurally diverse and currently detected by different diagnostic assays. This study sought to establish whole transcriptome RNA sequencing as single, comprehensive, and flexible platform for AML diagnostics. We developed HAMLET (Human AML Expedited Transcriptomics) as bioinformatics pipeline for simultaneous detection of fusion genes, small variants, tandem duplications, and gene expression with all information assembled in an annotated, user-friendly output file. Whole transcriptome RNA sequencing was performed on 100 AML cases and HAMLET results were validated by reference assays and targeted resequencing. The data showed that HAMLET accurately detected all fusion genes and overexpression of EVI1 irrespective of 3q26 aberrations. In addition, small variants in 13 genes that are often mutated in AML were called with 99.2% sensitivity and 100% specificity, and tandem duplications in FLT3 and KMT2A were detected by a novel algorithm based on soft-clipped reads with 100% sensitivity and 97.1% specificity. In conclusion, HAMLET has the potential to provide accurate comprehensive diagnostic information relevant for AML classification, risk assessment and targeted therapy on a single technology platform.