Recombinant Human R-Spondin 3 Protein

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RS03-100 包含以下产品
  • Recombinant Human R-Spondin 3 Protein 冻干粉 100µg/vial x 1
RS03-1000 包含以下产品
  • Recombinant Human R-Spondin 3 Protein 冻干粉 500µg/vial x 2
科途医学 科学家
名字
PhD

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我们的产品简化了实验流程，集成多种因子，无需单独优化，扩增潜力高，14天内细胞数量可达到1×10^6。适用于多种培养形式，包括基质胶、低吸附孔板和生物反应器悬浮培养。GMP级别生产条件下制备，批次质量稳定，试剂含量是常规市售干细胞培养基的2倍，实现极佳的成本效益比。让复杂的培养变得简单快速，让科研变得更高效。

概览
产品使用说明及支持信息
资源及文献引用
COA查询

概览

产品参数：

Source:

Human R-Spondin 3
(Gln22-His272)
Accession # Q9BXY4

N-terminus

 

C-terminus

Human HEK293 cell line, HEK293-derived human R-Spondin 3 protein.

Accession:

Q9BXY4

Purity:

>90%, by SDS-PAGE under reducing conditions.

Endotoxin Level:

<0.10 EU/μg of the protein by the LAL method.

Activity:

Measured by its ability to induce Topflash reporter activity in HEK293 reporter cells. The ED50 for this effect is 0.5-5.0ng/mL in the presence of 20 ng/mL Recombinant Wnt Surrogate Fc Chimera Protein (K2 Oncology, Catalog # WT01-100).

Structure:

Monomer

Predicted Molecular Weight

28.3 kDa (monomer).

SDS-PAGE

36-48 kDa, reducing conditions.

Sterile:

0.22μm sterile filtration.

Product Form:

Lyophilized powder.

Shipping & Storage:

The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below:

Ø  To the date of expiration, -20°C to -80°C as supplied.

Ø  3 months, -20°C to -80°C under sterile conditions after reconstitution.

Ø  1 month, 2 to 8 °C under sterile conditions after reconstitution.

Avoid repeated freeze-thaw cycles.

产品数据：
The purity of the recombinant human R-Spondin 3 protein was analyzed using SDS-PAGE under reducing conditions and stained using Coomassie blue.
Measured by its ability to induce Topflash reporter activity in HEK293 reporter cells. The ED50 for this effect is 0.5-5.0ng/mL in the presence of 20 ng/mL Recombinant Wnt Surrogate Fc Chimera Protein (K2 Oncology, Catalog # WT01-100)
产品背景：

R-Spondin 3 (RSPO3), also known as Cristin 1 or roof plate-specific spondin 3, is a secreted protein with a molecular weight of approximately 36 kDa. It shares around 40% amino acid identity with other members of the R-Spondin family. All R-Spondins act as positive modulators of Wnt/β-catenin signaling, but each exhibits a distinct expression pattern. RSPO3, like other R-Spondins, contains two adjacent cysteine-rich furin-like domains (amino acids 35-135), a potential N-glycosylation site (amino acid 36), a thrombospondin (TSP-1) motif (amino acids 147-207), and a region rich in basic residues (amino acids 211-269). The furin-like domains are sufficient for stabilizing β-catenin. RSPO3 shares high amino acid sequence identity within amino acids 21-209 with mouse, rat, equine, bovine, and canine RSPO3 (93%, 92%, 97%, 96%, and 92% identity, respectively).

In mice, RSPO3 is crucial for the development of the placental labyrinthine layer, likely by promoting vascular development through VEGF expression . It is also essential for the expression of Gcm1, a placenta-specific transcription factor. RSPO3 is often expressed by or located near endothelial cells in mouse embryos. It is found in various regions, including the roof plate, tail, somites, otic vesicles, cephalic mesoderm, truncus arteriosus, atrioventricular canal of the developing heart, and developing limbs.

R-Spondins regulate Wnt/β-catenin signaling by competing with the Wnt antagonist DKK-1 for binding to the Wnt co-receptors LRP-6 and Kremen, thereby reducing DKK-1-mediated internalization.

产品名称货号规格储存温度保质期
Recombinant Human R-Spondin 3 Protein RS03-100/1000100µg / 1mg-20°C / -80°C3个月

类型

细胞因子

物种

人类

应用

细胞培养 / 类器官培养

商标

OrganoPro™

产品使用说明及支持信息

在产品文档中查找支持信息和使用说明，或在下方探索更多

文档类型产品名称Catalog #
User manualRecombinant Human R-Spondin 3 Protein RS03-100 RS03-1000

资源及文献引用

相关资源及文献引用

Organoid drug screening report for a non-small cell lung cancer patient with EGFR gene mutation negativity: A case report and review of the literature
Pan, Yuetian, Hongshang Cui, and Yongbin Song | Frontiers in Oncology (2023)

Abstract:
Patients with non-small cell lung cancer (NSCLC) who carry epidermal growth factor receptor (EGFR) mutations can benefit significantly from EGFR tyrosine kinase inhibitors (EGFR TKIs). However, it is unclear whether patients without EGFR mutations cannot benefit from these drugs. Patient-derived tumor organoids (PDOs) are reliable in vitro tumor models that can be used in drug screening. In this paper, we report an Asian female NSCLC patient without EGFR mutation. Her tumor biopsy specimen was used to establish PDOs. The treatment effect was significantly improved by anti-tumor therapy guided by organoid drug screening.
Read More: https://doi.org/10.3389/fonc.2023.1109274

Identification of solamargine as a cisplatin sensitizer through phenotypical screening in cisplatin-resistant NSCLC organoids
Han, Yi,et al. | Frontiers in Pharmacology (2022)

Abstract:
Although Cisplatin (DDP) is a widely used first-line chemotherapy medication, DDP resistance is one of the main causes of treatment failure in advanced lung cancer. Therefore, it is urgent to identify DDP sensitizers and investigate the underlying molecular mechanisms. Here we utilized DDP-resistant organoids established from tumor biopsies of patients with relapsed lung cancers. In this study, we identified Solamargine as a potential DDP sensitizer through screening a natural product library. Mechanically, Solamargine induced G0/G1-phase arrest and apoptosis in DDP-resistant lung cancer cell lines. Gene expression analysis and KEGG pathway analysis indicated that the hedgehog pathway was suppressed by Solamargine. Moreover, Gli responsive element (GRE) reporter gene assay and BODIPY-cyclopamine binding assay showed that Solamargine inhibited the hedgehog pathway via direct binding to SMO protein. Interestingly, Solamargine and DDP showed a synergetic effect in inhibiting DDP-resistant lung cancer cell lines. Taken together, our work herein revealed Solamargine as a hedgehog pathway inhibitor and DDP-sensitizer, which might provide a new direction for further treatment of advanced DDP-resistant lung cancer patients.
Read More: https://doi.org/10.3389/fphar.2022.802168

An Artemisinin Derivative ART1 Induces Ferroptosis by Targeting the HSD17B4 Protein Essential for Lipid Metabolism and Directly Inducing Lipid Peroxidation.
Xie, Jingjing, et al. | CCS Chemistry (2022)

Abstract:
Artemisinin and its derivatives, commonly known as antimalarial drugs, have gradually come to be regarded as potential antitumor agents, although their cytotoxic efficacy and mechanisms of action remain to be settled. Herein, we report that an artemisinin analog, ART1, can potently induce ferroptosis in a subset of cancer cell lines. Structure–activity relationship (SAR) analysis reveals that both the endoperoxide moiety and the artemisinin skeleton are required for the antitumor activity of ART1. Aided with ART1-based small-molecule tools, chemical proteomic analysis identified the HSD17B4 protein as a direct target of ART1. HSD17B4 resides in peroxisomes and is an essential enzyme in the catabolism of very-long-chain fatty acids. Our results demonstrate that ART1 initiates ferroptosis through selective oxidation of the fatty acids in peroxisomes by hijacking the HSD17B4 protein without disturbing its enzymatic function, providing a promising mechanism to develop therapeutics for cancer treatment. Read More: https://doi.org/10.31635/ccschem.021.202000691

Pyrotinib in patients with HER2-amplified advanced non–small cell lung cancer: A prospective, multicenter, single-arm trial
Song, Zhengbo,et al. | Clinical Cancer Research (2022)

Abstract:
Purpose:
In this study, we aimed to evaluate the efficacy and safety of pyrotinib, a pan-HER inhibitor, in patients with HER2-amplified non–small cell lung cancer (NSCLC).
Patients and Methods:
In this prospective, multicenter, single-arm trial (ChiCTR1800020262), patients with advanced NSCLC with HER2 amplification, as determined by next-generation sequencing, were enrolled and administered pyrotinib orally at 400 mg per day. The primary endpoint was 6-month progression-free survival (PFS) rate. Other endpoints included objective response rate (ORR), disease control rate (DCR), PFS, overall survival (OS), and safety.
Results:
The enrolled cohort included 27 patients with HER2 amplification. The 6-month PFS rate was 51.9% [95% confidence interval (CI), 34.0–69.3]. The median PFS (mPFS) was 6.3 months (95% CI, 3.0–9.6 months), and median OS was 12.5 months (95% CI, 8.2–16.8 months). Pyrotinib elicited a confirmed ORR of 22.2% (95% CI, 10.6%−40.8%). Patients administered pyrotinib as first-line treatment achieved an mPFS of 12.4 months. Moreover, 30.8% of the patients who had progressed on EGFR tyrosine kinase inhibitor (TKI) responded to pyrotinib. Patients with brain metastases had an ORR of 40%. Treatment-related adverse events (TRAE) occurred in all patients (grade 3, 22.2%), but no grade 4 or higher TRAEs were documented. Diarrhea was the most frequent TRAE (all, 92.6%; grade 3, 7.4%). Loss of HER2 amplification was detected upon disease progression.
Conclusions:
Pyrotinib provided antitumor efficacy with a manageable safety profile in HER2-amplified patients with NSCLC.
Read More: https://doi.org/10.1158/1078-0432.CCR-21-2936

Glutamine synthetase licenses APC/C-mediated mitotic progression to drive cell growth
Zhao, Jiang-Sha,et al. | Nature Metabolism (2022)

Abstract:
Tumors can reprogram the functions of metabolic enzymes to fuel malignant growth; however, beyond their conventional functions, key metabolic enzymes have not been found to directly govern cell mitosis. Here, we report that glutamine synthetase (GS) promotes cell proliferation by licensing mitotic progression independently of its metabolic function. GS depletion, but not impairment of its enzymatic activity, results in mitotic arrest and multinucleation across multiple lung and liver cancer cell lines, patient-derived organoids and xenografted tumors. Mechanistically, GS directly interacts with the nuclear pore protein NUP88 to prevent its binding to CDC20. Such interaction licenses activation of the CDC20-mediated anaphase-promoting complex or cyclosome to ensure proper metaphase-to-anaphase transition. In addition, GS is overexpressed in human non-small cell lung cancer and its depletion reduces tumor growth in mice and increases the efficacy of microtubule-targeted chemotherapy. Our findings highlight a moonlighting function of GS in governing mitosis and illustrate how an essential metabolic enzyme promotes cell proliferation and tumor development, beyond its main metabolic function.
Read More: https://doi.org/10.1038/s42255-021-00524-2

Halofuginone sensitizes lung cancer organoids to cisplatin via suppressing PI3K/AKT and MAPK signaling pathways
Li, Hefei,et al. | Frontiers in Cell and Developmental Biology (2021)

Abstract:

Lung cancer is the leading cause of cancer death worldwide. Cisplatin is the major DNA-damaging anticancer drug that cross-links the DNA in cancer cells, but many patients inevitably develop resistance with treatment. Identification of a cisplatin sensitizer might postpone or even reverse the development of cisplatin resistance. Halofuginone (HF), a natural small molecule isolated from Dichroa febrifuga, has been found to play an antitumor role. In this study, we found that HF inhibited the proliferation, induced G0/G1 phase arrest, and promoted apoptosis in lung cancer cells in a dose-dependent manner. To explore the underlying mechanism of this antitumor effect of halofuginone, we performed RNA sequencing to profile transcriptomes of NSCLC cells treated with or without halofuginone. Gene expression profiling and KEGG analysis indicated that PI3K/AKT and MAPK signaling pathways were top-ranked pathways affected by halofuginone. Moreover, combination of cisplatin and HF revealed that HF could sensitize the cisplatin-resistant patient-derived lung cancer organoids and lung cancer cells to cisplatin treatment. Taken together, this study identified HF as a cisplatin sensitizer and a dual pathway inhibitor, which might provide a new strategy to improve prognosis of patients with cisplatin-resistant lung cancer.

Read More: https://doi.org/10.3389/fcell.2021.773048

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