Human TGFBR1 (TGF-beta receptor type-1) ELISA Kit

Name: Human TGFBR1 (TGF-beta receptor type-1) ELISA Kit
SKU: DEIA-FN1515
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

serum, plasma, cell culture supernatants, tissue homogenate

Species Reactivity

Human

Detection Method

Sandwich ELISA

Intended Use

For quantitative detection of Human TGFBR1 (TGF-beta receptor type-1) in serum, plasma, tissue homogenates and other biological fluids.

Contents of Kit

1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy

Storage

Store the unopened product at 2 - 8 °C. Do not use past expiration date.

Precision

Intra-Assay: CV<8%
Inter-Assay: CV<10%

Detection Range

0.156-10 ng/mL

Sensitivity

0.094 ng/mL

Standard Curve

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

miR-181b-induced SMAD7 downregulation controls granulosa cell apoptosis through TGF-beta signaling by interacting with the TGFBR1 promoter

JOURNAL OF CELLULAR PHYSIOLOGY

Authors: Yao, Wang; Pan, Zengxiang; Du, Xing; Zhang, Jinbi; Li, Qifa

Abstract

SMAD7 disrupts the TGF- signaling pathway by influencing TGFBR1 stability and by blocking the binding of TGFBR1 to SMAD2/3. In this study, we showed that SMAD7 attenuated the TGF- signaling pathway in ovarian granulosa cells (GCs) by regulating TGFBR1 transcriptional activity. To function as a transcription factor, SMAD7 downregulated the mRNA levels of TGFBR1 via direct binding to the SMAD-binding elements (SBEs) within the promoter region of pig TGFBR1. We also showed that SMAD7 enhanced porcine GC apoptosis by interrupting TGFBR1 and the TGF- signaling pathway. Interestingly, miR-181b, a microRNA that is downregulated during porcine follicular atresia, was identified to be directly targeting SMAD7 at its 3-UTR. By inhibiting SMAD7, miR-181b could inhibit GC apoptosis by activating the TGF- signaling pathway. Our findings provide new insights into the mechanisms underlying the regulation of the TGF- signaling pathway by SMAD7 and miR-181b.

Pathogenic effect of a TGFBR1 mutation in a family with Loeys-Dietz syndrome

MOLECULAR GENETICS & GENOMIC MEDICINE

Authors: Cozijnsen, Luc; Plomp, Astrid S.; Post, Jan G.; Pals, Gerard; Bogunovic, Natalija; Yeung, Kak K.; Niessen, Hans W. M.; Goumans, Marie-Jose T. H.; Barge-Schaapveld, Daniela Q. C. M.; Micha, Dimitra

Abstract

Background Thoracic aortic aneurysms and dissections (TAAD) may have a heritable cause in up to 20% of cases. We aimed to investigate the pathogenic effect of a TGFBR1 mutation in relation to TAAD. Methods Co-segregation analysis was performed followed by functional investigations, including myogenic transdifferentiation. Results The c.1043G>A TGFBR1 mutation was found in the index patient, in a deceased brother, and in five presymptomatic family members. Evidence for pathogenicity was found by the predicted damaging effect of this mutation and the co-segregation in the family. Functional analysis with myogenic transdifferentiation of dermal fibroblasts to smooth muscle-like cells, revealed increased myogenic differentiation in patient cells with the TGFBR1 mutation, shown by a higher expression of myogenic markers ACTA2, MYH11 and CNN1 compared to cells from healthy controls. Conclusion Our findings confirm the pathogenic effect of the TGFBR1 mutation in causing TAAD in Loeys-Dietz syndrome and show increased myogenic differentiation of patient fibroblasts.