Human Vascular Endothelial Growth Factor Receptor 1 / VEGFR1 (FLT1) Peptide (OVA)

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Especificaciones del producto

Proteins and Peptides

Vascular Endothelial Growth Factor Receptor 1 / VEGFR1 (FLT1)

Synthetic

Activity: Not tested
Sequence Fragment: Ala1312-Asn1328

Human

OVA

Synthetic

> 90%

100 µg

200 µg

500 µg

1 mg

5 mg

Lyophilized

WB, SDS-PAGE

Prior to lyophilization: PBS, pH 7.4.

Shipped within 5-7 working days.

Store lyophilized form at 2-8°C for up to 1 month. For longer periods, store lyophilized or liquid at -80°C. Avoid repeated freeze–thaw cycles.

No

FLT,FLT-1,VEGFR1,VEGFR-1,Vascular permeability factor receptor,Fms-like tyrosine kinase 1,Vascular endothelial growth factor receptor 1

Protein FLT1

RUO

THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION.
To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex.
Concentration: Prior to lyophilization: 200 µg/ml

Background

Fms related receptor tyrosine kinase 1 (FLT1) FLT1, also known as vascular endothelial growth factor receptor 1 (VEGFR1), is a transmembrane tyrosine kinase receptor that binds vascular endothelial growth factors (VEGFs) and placental growth factor (PlGF). FLT1 plays a crucial role in angiogenesis, vascular development, and inflammation by regulating endothelial cell proliferation, migration, and survival. Structurally, FLT1 consists of an extracellular ligand-binding domain with seven immunoglobulin-like loops, a transmembrane domain, and an intracellular kinase domain. FLT1 can function as a signaling receptor or a decoy receptor, depending on its membrane-bound or soluble isoforms, modulating VEGF availability and signaling intensity. It is highly expressed in endothelial cells and trophoblasts, contributing to processes such as placental development and vascular remodeling. Dysregulation of FLT1 is implicated in pathological conditions, including cancer, where it promotes tumor angiogenesis, and preeclampsia, where excessive FLT1 activity leads to impaired placental and vascular function. Its dual role as a regulator of VEGF signaling and a therapeutic target underscores its importance in both physiological and pathological angiogenesis.

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