Mouse Bone Morphogenetic Protein 4, BMP4 ELISA Kit
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Induces cartilage and bone formation. Acts in concert with PTHLH/PTHRP to stimulate ductal outgrowth during embryonic mammary development and to inhibit hair follicle induction.
Fully tested in-house by ABMIUM, or supported by an advanced validation report from a partner reviewed by ABMIUM. Highest confidence. Non-conformities fully supported under the ABMIUM Product Promise.
Quality verified. Independent collaborator or expected-performance data available. Product meets ABMIUM quality standards.
Expected to work based on structural and biochemical data. Not yet directly tested by ABMIUM or a collaborator. No non-conformity support for this combination.
Not recommended for this application or species/sample combination. This may indicate either evidence of unsuitability or that the combination has not been tested and therefore cannot currently be recommended.
Evidence status by application and model.
| Evidence | Serum | Plasma | Cell culture supernatants | Ascites | Tissue homogenates |
|---|---|---|---|---|---|
| Compatibility |
This product is manufactured by BT LAB and sold through ABMIUM without relabelling.
ABMIUM supports global orders. Availability, shipping requirements and applicable import arrangements are confirmed before fulfilment where required.
Yes. Send your target, sample, application and experimental conditions through ABMIUM MATCH or technical support.
Unless the listing expressly states otherwise, ABMIUM products are supplied for research use only and are not for diagnostic or therapeutic use.
Bone morphogenetic protein 4 (BMP4/BMP-4) is a secreted TGF-beta superfamily growth factor involved in developmental signalling and tissue differentiation. ABMIUM catalogue products linked below support research on BMP4 biology.
Biological function: Bone morphogenetic protein 4 (BMP4) is a TGF-beta superfamily growth factor with key roles in developmental patterning, differentiation, osteogenesis and vascular development. Canonical BMP4 signalling occurs through type I and type II BMP receptors and activates SMAD1/5/8-dependent transcription, while additional non-canonical pathways can also contribute.
