p90 RSK (Phospho-Ser380) ELISA Kit

Name: p90 RSK (Phospho-Ser380) ELISA Kit
SKU: DEIA-XYA1396
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 p90 RSK (Phospho-Ser380) Colorimetric Cell-Based ELISA Kit allows for the qualitative detection of p90 RSK (Phospho-Ser380) and the effects that certain stimulation conditions have on p90 RSK (Phospho-Ser380) expression in different cell lines.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 2 Plates.
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-p90 RSK (Phospho-Ser380) Antibody (Rabbit Polyclonal) 60 μL (100x) Red.
7. 100x Anti-p90 RSK Antibody (Rabbit Polyclonal) 60 μL (100x) Purple.
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal) 60 μL (100x) Green.
9. HRP-Conjugated Anti-Rabbit IgG Antibody, 12 mL (1x), Glass.
10. HRP-Conjugated Anti-Mouse IgG Antibody, 12 mL (1x), Glass.
11. Primary Antibody Diluent, 12 mL (1x), Clear.
12. Ready-to-Use Substrate, 12 mL (1x), Brown.
13. Stop Solution, 12 mL (1x), Clear.
14. Crystal Violet Solution, 12 mL (1x), Glass.
15. SDS Solution, 24 mL (1x), Clear.
16. 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

Chemically Induced Degradation of Anaplastic Lymphoma Kinase (ALK)

JOURNAL OF MEDICINAL CHEMISTRY

Authors: Powell, Chelsea E.; Gao, Yang; Tan, Li; Donovan, Katherine A.; Nowak, Radoslaw P.; Loehr, Amanda; Bahcall, Magda; Fischer, Eric S.; Janne, Pasi A.; George, Rani E.; Gray, Nathanael S.

Abstract

We present the development of the first small molecule degraders that can induce anaplastic lymphoma kinase (ALK) degradation, including in non-small-cell lung cancer (NSCLC), anaplastic large-cell lymphoma (ALCL), and neuroblastoma (NB) cell lines. These degraders were developed through conjugation of known pyrimidine-based ALK inhibitors, TAE684 or LDK378, and the cereblon ligand pomalidomide. We demonstrate that in some cell types degrader potency is compromised by expression of drug transporter ABCB1. In addition, proteomic profiling demonstrated that these compounds also promote the degradation of additional kinases including PTK2 (FAK), Aurora A, FER, and RPS6KA1 (RSK1).

Genomic profiling of Sezary syndrome identifies alterations of key T cell signaling and differentiation genes

NATURE GENETICS

Authors: Wang, Linghua; Ni, Xiao; Covington, Kyle R.; Yang, Betty Y.; Shiu, Jessica; Zhang, Xiang; Xi, Liu; Meng, Qingchang; Langridge, Timothy; Drummond, Jennifer; Donehower, Lawrence A.; Doddapaneni, Harshavardhan; Muzny, Donna M.; Gibbs, Richard A.; Wheeler, David A.; Duvic, Madeleine

Abstract

Sezary syndrome is a rare leukemic form of cutaneous T cell lymphoma characterized by generalized redness, scaling, itching and increased numbers of circulating atypical T lymphocytes. It is rarely curable, with poor prognosis. Here we present a multiplatform genomic analysis of 37 patients with Sezary syndrome that implicates dysregulation of cell cycle checkpoint and T cell signaling. Frequent somatic alterations were identified in TP53, CARD11, CCR4, PLCG1, CDKN2A, ARID1A, RPS6KA1 and ZEB1. Activating CCR4 and CARD11 mutations were detected in nearly one-third of patients. ZEB1, encoding a transcription repressor essential for T cell differentiation, was deleted in over one-half of patients. IL32 and IL2RG were overexpressed in nearly all cases. Our results demonstrate profound disruption of key signaling pathways in Sezary syndrome and suggest potential targets for new therapies.