ASK1 ELISA Kit

Name: ASK1 ELISA Kit
SKU: DEIA-XYA234
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 ASK1 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor ASK1 protein expression profile in cells. The kit can be used for measuring the relative amounts of ASK1 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on ASK1.

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-ASK1 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 variation in 1253 immune and inflammation genes and risk of non-Hodgkin lymphoma

BLOOD

Authors: Cerhan, James R.; Ansell, Stephen M.; Fredericksen, Zachary S.; Kay, Neil E.; Liebow, Mark; Call, Timothy G.; Dogan, Ahmet; Cunningham, Julie M.; Wang, Alice H.; Liu-Mares, Wen; Macon, William R.; Jelinek, Diane; Witzig, Thomas E.; Habermann, Thomas M.; Slager, Susan L.

Abstract

Smaller-scale evaluations suggest that common genetic variation in candidate genes related to immune function may predispose to the development of non-Hodgkin lymphoma (NHL). We report an analysis of variants within genes associated with immunity and inflammation and risk of NHL using a panel of 9412 single-nucleotide polymorphisms (SNPs) from 1253 genes in a study of 458 patients with INK and 484 frequency-matched controls. We modeled haplotypes and risk of NHL, as well as the main effects for all independent SNPs from a gene in multivariate logistic regression models; we separately report results for nonsynonymous (ns) SNPs. In gene-level analyses, the strongest findings (P <= .001) were for CREB1, FGG, MAP3K5, RIPK3, LSP1, TRAF1, DUSP2, and ITGB3. In nsSNP analyses, the strongest findings (P <= .01) were for ITGB3 L59P (odds ratio [OR] = 0.66; 95% confidence interval [CI] 0.52-0.85), TLR6 V427A (OR = 5.20; Cl 1.77-15.3), SELPLG M264V (OR = 3.20; Cl 1.48-6.91), UNC84B G671S (OR = 1.50; Cl 1.12-2.00), B3GNT3 H328R (OR = 0.74; Cl 0.59-0.93), and BAT2 V1883L (OR = 0.64; Cl 0.45-0.90). Our results suggest that genetic variation in genes associated with immune response (TRAF1, RIPK3, BAT2, and TLR6), mitogen-activated protein kinase (MAPK) signaling (MAP3K5, DUSP2, and CREB1), lymphocyte trafficking and migration (B3GNT3, SELPLG, and LSP1), and coagulation pathways (FGG and ITGB3) may be important in the etiology of NHL, and should be prioritized in replication studies.

Neuronal Activity, TGF beta-Signaling and Unpredictable Chronic Stress Modulate Transcription of Gadd45 Family Members and DNA Methylation in the Hippocampus

CEREBRAL CORTEX

Authors: Grassi, Daniela; Franz, Henriette; Vezzali, Riccardo; Bovio, Patrick; Heidrich, Stefanie; Dehghanian, Fariba; Lagunas, Natalia; Belzung, Catherine; Krieglstein, Kerstin; Vogel, Tanja

Abstract

Neuronal activity is altered in several neurological and psychiatric diseases. Upon depolarization not only neurotransmitters are released but also cytokines and other activators of signaling cascades. Unraveling their complex implication in transcriptional control in receiving cells will contribute to understand specific central nervous system (CNS) pathologies and will be of therapeutically interest. In this study we depolarized mature hippocampal neurons in vitro using KCl and revealed increased release not only of brain-derived neurotrophic factor (BDNF) but also of transforming growth factor beta (TGFB). Neuronal activity together with BDNF and TGFB controls transcription of DNA modifying enzymes specifically members of the DNA-damage-inducible (Gadd) family, Gadd45a, Gadd45b, and Gadd45g. MeDIP followed by massive parallel sequencing and transcriptome analyses revealed less DNA methylation upon KCl treatment. Psychiatric disorder-related genes, namely Tshz1, Foxn3, Jarid2, Per1, Map3k5, and Arc are transcriptionally activated and demethylated upon neuronal activation. To analyze whether misexpression of Gadd45 family members are associated with psychiatric diseases, we applied unpredictable chronic mild stress (UCMS) as established model for depression to mice. UCMS led to reduced expression of Gadd45 family members. Taken together, our data demonstrate that Gadd45 family members are new putative targets for UCMS treatments.