Recombinant Human Vascular Endothelial Growth Inhibitor

• Cat.No.: TNFSF15-27H
• Product Overview: Recombinant human VEGI-192 produced inE. coliis a single, non-glycosylated polypeptide chain containing 192 amino acids and having a molecular mass of 21.858 kDa.

Specification

• Cat. No.: TNFSF15-27H
• Description: Vascular endothelial growth inhibitor (VEGI; TNFSF-15) is a new member of the tumor necrosis factor family. VEGI is predominantly an endothelial cell-specific gene, and recombinant VEGI is a potent inhibitor of endothelial cell proliferation, angiogenesis and tumor growth. VEGI exerts two activities on endothelial cells: early G1 arrest of G0/G1-cells responding to growth stimuli, and programmed death of proliferating cells. These activities are highly specific to endothelial cells. VEGI is also able to regulate the expression of several important genes involved in angiogenesis. These findings are consistent with the view that VEGI functions as an autocrine cytokine to inhibit angiogenesis and stabilize the vasculature.
• Purity: >95% by SDS-PAGE and RP-HPLC.
• Formulation: Lyophilized after extensive dialysis against 0.5M NaCl, 50mM Tris-HCl buffer, pH 7.5.
• Specific Activity: The ED50 as determined by the dose-dependant inhibition of the proliferation of HUVEC (Human Umbilical Vein Endothelial Cells) is less than 5μg/ml.
• Endotoxin: Less than 0.1 ng/µg (1 IEU/µg) of rHuVEGI
• Reconstitution: It is recommended to reconstitute the lyophilized VEGI-192 in sterile 18MΩ-cm H₂O not less than 100µg/ml, which can then be further diluted to other aqueous solutions.
• Storagee: Lyophilized VEGI-192 although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution VEGI-192 should be stored at 4°C between 2-7 days and for future use below -18°C. For long-term storage it is recommended to add a carrier protein (0.1% HSA or BSA). Aliquot to avoid repeated freeze-thaw cycles.

Gene Information

• Gene Name: TNFSF15
• Synonyms: MGC129934; MGC129935; TL1; TL1A; VEGI; VEGI192A; Tumor necrosis factor ligand superfamily member 15; Vascular endothelial cell growth inhibitor; TNF ligand-related molecule 1; TNF15; TNFSF15; TL-1; VEGI-192; tumor necrosis factor (ligand) superfamily, member 15
• Gene ID: 9966
• mRNA Refseq: NM_005118.2
• Protein Refseq: NP_005109.2
• MIM: 604052
• UniProt ID: O95150
• Chromosome Location: 9q32
• Pathway: Cytokine-cytokine receptor interaction
• Function: Cytokine activity, Tumor necrosis factor receptor binding

Reviews

03/21/2022

They keep up with the latest research findings and continually refine their product based on customer feedback and emerging scientific trends.

05/01/2021

Their prompt assistance and prompt response can swiftly resolve any challenges, enabling smooth experimentation and maintaining the integrity of the results.

10/01/2017

Their knowledgeable support team is well-equipped to address specific inquiries, suggest experimental protocols, and provide guidance throughout the entire research process.

Q&As

How does TNFSF15 interact with other components of the immune system?

TNFSF15 interacts with receptors on immune cells, influencing their activity and contributing to the overall regulation of immune responses.

Are there any current clinical trials targeting TNFSF15 for autoimmune disease treatments?

Several clinical trials are underway to evaluate the efficacy and safety of therapies targeting TNFSF15 in autoimmune diseases.

Are there any diagnostic implications of TNFSF15 in autoimmune disorders?

TNFSF15 levels may serve as a biomarker for certain autoimmune conditions, aiding in the diagnosis and monitoring of disease progression.

Can TNFSF15 be a potential target for novel drug development in autoimmune diseases?

TNFSF15 is considered a promising target for drug development, and ongoing research aims to identify compounds that modulate its activity effectively.

How does TNFSF15 contribute to the pathogenesis of inflammatory bowel disease (IBD)?

In IBD, TNFSF15 is believed to be involved in the inflammation process, contributing to the chronic nature of the disease.