Human/Mouse/Rat Activin A ELISA Kit (DEIA2735)

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

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cell culture supernatants, serum, plasma, saliva
Species Reactivity
Human, Mouse, Rat
Intended Use
For the quantitative determination of human, mouse, or rat Activin A concentrations in cell culture supernates, serum, plasma, and saliva.
Contents of Kit
1. Streptavidin Microplate
2. Activin A Biotinylated Antibody
3. Activin A Conjugate
4. Activin A Standard
5. Assay Diluent
6. Calibrator Diluent4
7. Wash Buffer Concentrate
8. Color Reagent A
9. Color Reagent B
10. Stop Solution
Store at 2-8°C. Do not use past kit expiration date.
Intra-assay Precision: 4.2%-4.4%
Inter-assay Precision: 4.7%-7.9%
Detection Range
0.75-7.85 pg/mL
3.67 pg/mL


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Long non-coding RNA NAPIL6 promotes tumor progression and predicts poor prognosis in prostate cancer by targeting Inhibin-beta A


Authors: Zheng, Yuxiao; Gao, Yiren; Li, Xiao; Si, Shuhui; Xu, Haoxiang; Qi, Feng; Wang, Jun; Cheng, Gong; Hua, Lixin; Yang, Haiwei

Background/purpose: Long non-coding RNAs (lneRNAs) have emerged as key molecules in initiation and progression of prostate cancer (PCa). In this study, we aimed to explore the role of lncRNA NAP1L6 in the development and progression of PCa. Materials and methods: We identified that lncRNA NAP1L6 was over-expressed both in PCa tissues and cell lines by gene expression array profiling. The expression level of NAP1L6 in 75 PCa tissues and adjacent tissues was detected by RT-PCR. Next, the correlations between NAP1L6 expression and clinical features of patients with PCa were analyzed by paired i-test or chi-squared test, and its association with patient prognosis was assessed by the Kaplan-Meier method. The effects of NAP1L6 on PC-3 and 22RV1 cells were evaluated by Cell Counting Kit-8 (CCK-8), migration, invasion, and colony formation assays. Further analysis of the results of the microarray was performed to find downstream gene of NAP1L6. Cell function experiments were performed in order to explore the relationship between NAP1L6 and Inhibin-beta A (INHBA) and the specific mechanism by which INHBA affects the development of PCa. Results: Using microarray analysis, we identified 412 lncRNAs and 1245 m RNAs to be significantly differentially expressed in three PCa samples when compared with adjacent nontumor tissues (ANTT) (fold-change >= 2.0 or <= 0.5, P<0.05, false discovery rate (FDR) <0.05). NAP1L6 expression was upregulated in PCa tissues and cell lines (both P<0.05) compared with ANTT. Besides, high expression level of NAPIL6 promotes PCa cell proliferation, migration, and invasion (all P<0.05), and is significantly associated with larger tumor diameter, distant metastasis, and shorter survival time (all P<0.05). We found that NAP1L6 promoted the expression of INHBA (P<0.05), and knockdown of NAP1L6 led to the reduction of PCa cell migration, invasion, and proliferation by regulating the expression of INHBA (all P<0.05). Conclusion: lncRNA NR6A1 might play an oncogenic role in PCa initiation and progression by regulating the expression of INHBA, and might act as a novel prognostic biomarker for PCa treatment.

Genome-wide association study for colorectal cancer identifies risk polymorphisms in German familial cases and implicates MAPK signalling pathways in disease susceptibility


Authors: Lascorz, Jesus; Forsti, Asta; Chen, Bowang; Buch, Stephan; Steinke, Verena; Rahner, Nils; Holinski-Feder, Elke; Morak, Monika; Schackert, Hans K.; Goergens, Heike; Schulmann, Karsten; Goecke, Timm; Kloor, Matthias; Engel, Cristoph; Buettner, Reinhard; Kunkel, Nelli; Weires, Marianne; Hoffmeister, Michael; Pardini, Barbara; Naccarati, Alessio; Vodickova, Ludmila; Novotny, Jan; Schreiber, Stefan; Krawczak, Michael; Broering, Clemens D.; Voelzke, Henry; Schafmayer, Clemens; Vodicka, Pavel; Chang-Claude, Jenny; Brenner, Hermann; Burwinkel, Barbara; Propping, Peter; Hampe, Jochen; Hemminki, Kari

Genetic susceptibility accounts for similar to 35% of all colorectal cancer (CRC). Ten common low-risk variants contributing to CRC risk have been identified through genome-wide association studies (GWASs). In our GWAS, 610 664 genotyped single-nucleotide polymorphisms (SNPs) passed the quality control filtering in 371 German familial CRC patients and 1263 controls, and replication studies were conducted in four additional case-control sets (4915 cases and 5607 controls). Known risk loci at 8q24.21 and 11q23 were confirmed, and a previously unreported association, rs12701937, located between the genes GLI3 (GLI family zinc finger 3) and INHBA (inhibin, beta A) [P = 1.1 x 10(-3), odds ratio (OR) 1.14, 95% confidence interval (CI) 1.05-1.23, dominant model in the combined cohort], was identified. The association was stronger in familial cases compared with unselected cases (P = 2.0 x 10(-4), OR 1.36, 95% CI 1.16-1.60, dominant model). Two other unreported SNPs, rs6038071, 40 kb upstream of CSNK2A1 (casein kinase 2, alpha 1 polypeptide) and an intronic marker in MYO3A (myosin IIIA), rs11014993, associated with CRC only in the familial CRC cases (P = 2.5 x 10(-3), recessive model, and P = 2.7 x 10(-4), dominant model). Three software tools successfully pointed to the overrepresentation of genes related to the mitogen-activated protein kinase (MAPK) signalling pathways among the 1340 most strongly associated markers from the GWAS (allelic P value < 10(-3)). The risk of CRC increased significantly with an increasing number of risk alleles in seven genes involved in MAPK signalling events (P-trend = 2.2 x 10(-16), ORper allele = 1.34, 95% CI 1.11-1.61).

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