Sample
Serum, plasma, cell culture supernatant and other biological samples
Intended Use
In vitro quantitative determination of SEMA3F concentrations in serum, plasma, cell culture supernatant and other biological samples.
Contents of Kit
1. ELISA Microplate(Dismountable), 8×12. Storage Condition for Opened Kit: Put the rest strips into a sealed foil bag with the desiccant. Stored for 1 month at 2-8°C. Stored for 12 month at -20°C.
2. Lyophilized Standard, 2vial. Storage Condition for Opened Kit: Put the rest standards into a desiccant bag. Stored for 1 month at 2-8°C. Stored for 12 month at -20°C.
3. Biotin-labeled Antibody(Concentrated, 100×), 120ul, 2-8°C (Avoid Direct Light)
4. HRP-Streptavidin Conjugate(SABC, 100×), 120ul, 2-8°C (Avoid Direct Light)
5. TMB Substrate, 10ml, 2-8°C (Avoid Direct Light)
6. Sample Dilution Buffer, 20ml, 2-8°C
7. Antibody Dilution Buffer, 10ml, 2-8°C
8. SABC Dilution Buffer, 10ml, 2-8°C
9. Stop Solution, 10ml, 2-8°C
10. Wash Buffer(25×), 30ml, 2-8°C
11. Plate Sealer, 5 pieces
12. Product Description. 1 copy
Note: The liquid reagent bottle contains slightly more reagent than indicated on the label. Please use pipette accurately measure and do proportional dilution.
Storage
2-8°C (for sealed box), please do not freeze! See kit label for expiry date
Performance Characteristics
Perform the stability test for the sealed kit at 37°C and 2-8°C and get relevant data.
Precision
Intra-assay Precision: samples with low, medium and high concentration are tested 20 times on same plate.
Inter-assay Precision: samples with low, medium and high concentration are tested 20 times on three different plates.
Detection Range
0.156-10ng/ml
General Description
Semaphorin 3F (SEMA3F) is a member of the semaphorin III family of secreted signaling proteins that are involved in axon guidance during neuronal development. SEMA3F contains an N-terminal Sema domain, an immunoglobulin loop and a C-terminal basic domain. SEMA3F is expressed by the endothelial cells where it was found to act in an autocrine fashion to induce apoptosis, inhibit cell proliferation and survival, and function as an anti-tumorigenic agent. Diseases associated with SEMA3F include Neuroma and Megacolon.
Standard Curve
This product has been tested by Quality Control Department and meets performance specifications mentioned in the manual. (The humidity in the laboratory is 20%-60%, and the temperature is 18°C -25°C. TMB was balanced to 37°C before color development, and incubated at 37°C for 15 minutes in the dark after adding the enzyme label plate holes.)
The following assay data are provided for reference, since experimental environment and operation are different. The establishment of standard curve depends on your own assay.
Citations
Publication ()
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Semaphorin 3A and 3F Promote Lumen Expansion in TIE2-Mutated Venous Malformation
Schrenk S, Sherpa C, Bischoff LJ, Cai Y, Boscolo E.
Arterioscler Thromb Vasc Biol2025 DecPubMed ID:41127911Read Article
Applications: ELISA
Reactive species: Human
"Abstract: Background:Venous malformations (VMs) are developmental defects of the vasculature characterized by tremendously enlarged and dysfunctional veins. Gain-of-function somatic mutations in TIE2 (endothelial tyrosine kinase receptor) have been identified as the leading driver of VM pathogenesis. The aim of this study was to determine whether the aberrant venous lumen expansion is caused by recruitment of wild-type (WT) endothelial cells (EC) to the lesion or by TIE2-mutant EC clonal expansion.
Methods: To investigate the contribution of TIE2-mutant EC and WT EC to the aberrant venous lumen expansion, we used a xenograft murine model of VM generated with a combination of TIE2-mutant EC and WT EC. To perform longitudinal studies, we used a 3-dimensional fibrin gel lumen formation assay and a migration assay, both using WT EC in competition or confrontation with TIE2-mutant EC. To investigate the mechanisms implicated in VM lumen expansion, we used RNA-sequencing and short-hairpin RNA silencing in the TIE2-mutant EC.
Results: We demonstrate here that in the VM xenograft model, the aberrant blood vessels were lined almost exclusively by TIE2-mutant EC, and WT EC were rarely found. Functionally, the TIE2-mutant EC exerted a competitive advantage over WT EC by inhibiting WT EC sprouting. In line with these findings, TIE2-mutant EC promoted repulsion of WT EC. Short-hairpin RNA-mediated silencing of Sema (Semaphorin) 3A or Sema3F in TIE2-mutant EC rescued this chemorepellent phenotype and restored the ability of WT EC to migrate, sprout, and form lumens. Furthermore, knockdown of Sema3A or Sema3F in TIE2-mutant EC normalized the blood vessel size in vivo.
Conclusions: Our results demonstrate that WT EC are not recruited to the aberrant veins, suggesting that VM pathogenesis is fueled by clonal expansion of TIE2-mutant EC. Mechanistically, we show that Sema3A and Sema3F are overexpressed in TIE2-mutant EC and play a crucial role in the pathological vascular lumen expansion in VM."
Article snippet: Sema3A and Sema3F protein levels were quantified using a total of 20 µg of protein lysate. The following ELISA assays were utilized according to the manufacturer’s instructions: Sema 3A (***) and Sema3F (Creative Diagnostics, cat DEIA-FN1341). 
Figure 1. Chemorepellent Sema (Semaphorin) 3A/Sema3F are overexpressed in TIE2 (endothelial tyrosine kinase receptor)-mutant endothelial cells (EC).
COA
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