Chk1 ELISA Kit

Name: Chk1 ELISA Kit
SKU: DEIA-XYA407
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

Detection Method

Indirect ELISA

Intended Use

The Chk1 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor Chk1 protein expression profile in cells. The kit can be used for measuring the relative amounts of Chk1 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on Chk1.

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-Chk1 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

Genetic variants of DNA repair-related genes predict efficacy of TAS-102 in patients with refractory metastatic colorectal cancer

ANNALS OF ONCOLOGY

Authors: Suenaga, M.; Schirripa, M.; Cao, S.; Zhang, W.; Yang, D.; Murgioni, S.; Rossini, D.; Marmorino, F.; Mennitto, A.; Ning, Y.; Okazaki, S.; Berger, M. D.; Miyamoto, Y.; Gopez, R., Jr.; Barzi, A.; Yamaguchi, T.; Loupakis, F.; Lenz, H. -J.

Abstract

Background: Tri-phosphorylated trifluridine (FTD) incorporation into DNA is TAS-102's main anti-tumor action. We tested whether genetic polymorphisms in homologous recombination (HR) and cell cycle checkpoint pathway for DNA repair is associated with outcomes in refractory metastatic colorectal cancer (mCRC) patients treated with TAS-102. Patients and methods: We analyzed genomic DNA extracted from 233 samples of three cohorts: an evaluation cohort of 52 patients receiving TAS-102, a validation cohort of 129 patients receiving TAS-102 and a control cohort of 52 patients receiving regorafenib. Single nucleotide polymorphisms of genes involved in HR (ATM, BRCA1, BRCA2, XRCC3, FANCD2, H2AX, RAD51) and cell cycle checkpoint (ATR, CHEK1, CHEK2, CDKN1A, TP53, CHE1, PIN1, PCNA) were analyzed by PCR-based direct sequencing. Results: In univariate analysis for the evaluation cohort, patients with any G allele in ATM rs609429 had longer overall survival (OS) than those with the C/C variant (8.7 vs. 4.4 months, HR 0.37, 95% CI: 0.14-0.99, P = 0.022). Patients carrying any A allele in XRCC3 rs861539 had significantly longer progression-free survival (PFS) (3.8 vs. 2.3 months, HR 0.44, 95% CI: 0.21-0.92, P = 0.024) and OS (15.6 vs. 6.3 months, HR 0.25, 95% CI: 0.08-0.79, P = 0.012) than those with the G/G variant. In multivariable analysis, ATM rs609429 remained significant for OS (P = 0.020). In the validation cohort, patients having ATM rs609429 with any G allele showed longer OS and PFS; the G/A variant in XRCC3 rs861539 showed longer OS, though without statistical significance. Conclusion: Genetic variants in the HR pathway may predict clinical outcome in mCRC patients receiving TAS-102.

Actionable co-alterations in breast tumors with pathogenic mutations in the homologous recombination DNA damage repair pathway

BREAST CANCER RESEARCH AND TREATMENT

Authors: Heeke, Arielle L.; Xiu, Joanne; Elliott, Andrew; Korn, W. Michael; Lynce, Filipa; Pohlmann, Paula R.; Isaacs, Claudine; Swain, Sandra M.; Vidal, Gregory; Schwartzberg, Lee S.; Tan, Antoinette R.

Abstract

Purpose Homologous recombination (HR)-deficient breast tumors may have genomic alterations that predict response to treatment with PARP inhibitors and other targeted therapies. Methods Comprehensive molecular profiles of 4647 breast tumors performed at Caris Life Sciences using 592-gene NGS were reviewed to identify somatic pathogenic mutations in HR genesARID1A, ATM, ATRX, BAP1, BARD1, BLM, BRCA1/2, BRIP1, CHEK1/2, FANCA/C/D2/E/F/G/L, KMT2D, MRE11, NBN, PALB2, RAD50/51/51B,andWRN,as well as 41 markers that may be associated with treatment response to targeted anticancer therapies. Results 17.9% of breast tumors had HR mutations (HR-MT, 831/4647) [ER/PR+ , HER2- 18.3%,n = 2183; TNBC 18.2%,n = 1568; ER/PR+ , HER2+ 15.6%,n = 237; ER/PR-, HER2+ 12.9%,n = 217; unknownn = 442]. Mean TMB was higher for HR-MT tumors across subtypes (9.2 mut/Mb vs 7.6 h-wild type (HR-WT),p <= 0.0001) and independent of microsatellite status. MSI-H/dMMR was more frequent among HR-MT tumors (2.1% HR-MT vs 0.2% HR-WT,p <= 0.0001), as was tumor PD-L1 overexpression (13.2% HR-MT vs 11.0% HR-WT,p = 0.08). Additional co-alterations were similar between HR-MT and HR-WT, with the exception ofPIK3CA(30.3% HR-WT vs 26.4% HR-MT,p = 0.024) andAKT1(3.7% HR-WT vs 2.1% HR-MT,p = 0.021). AR overexpression andPIK3CAmutations were more common among ER/PR+ tumors. ERBB2 mutations were seen in both HER2+ and HER2- tumors. Conclusions HR-MT was common across breast cancer subtypes and co-occurred more frequently with markers of response to immunotherapy (MSI-H/dMMR, TMB) compared to HR-WT tumors. Mutations were identified in both HR-MT and HR-WT tumors that suggest other targets for treatment. Clinical trials combining HRD-targeted agents and immunotherapy are underway and could be enriched through comprehensive molecular profiling.