| Cat # | Size | Price | Quantity | |
|---|---|---|---|---|
| 114401 | 25 μg | $45 | ||
| 114402 | 100 μg | $90 |
| Clone | 9F10 |
|---|---|
| Application | Flow Cytometry |
| Reactivity | Human |
| Format | Purified |
| Target Name | CD49d, VLA-4 α, Integrin α4, ITGA4 |
| Isotype | Mouse IgG1 |
| Antibody Type | Monoclonal |
| Regulatory Status | RUO |
| Formulation | Phosphate-buffered solution, pH 7.2, containing 0.09% sodium azide |
| Protein Concentration | 0.5 mg/mL |
| Storage&Handling | The antibody solution should be stored between 2°C and 8°C |
| Isotype Controls | 301401 |
| Antibody Family | Human Antibodies |
| See All Formats | Clone 9F10 |
CD49d, also known as integrin α4, is a cell surface adhesion molecule expressed on leukocytes including lymphocytes, monocytes, and eosinophils. It plays a central role in immune cell trafficking by mediating adhesion to vascular endothelium and facilitating transmigration into tissues during immune surveillance and inflammation. CD49d pairs with β1 (CD29) or β7 integrins to form the heterodimers α4β1 (VLA-4) and α4β7, each with distinct tissue-homing functions.
Structurally, CD49d is a type I transmembrane glycoprotein with a large extracellular domain responsible for ligand binding, a single-pass transmembrane region, and a short cytoplasmic tail that links to intracellular signaling and cytoskeletal machinery. Its principal ligands include VCAM-1 (vascular cell adhesion molecule-1) and fibronectin for α4β1, and MAdCAM-1 (mucosal addressin cell adhesion molecule-1) for α4β7, enabling tissue-specific adhesion and migration.
In disease, CD49d contributes to chronic inflammation and autoimmune disorders such as multiple sclerosis and inflammatory bowel disease by promoting leukocyte infiltration into target tissues. It is also implicated in cancer, particularly in leukemias, where high CD49d expression correlates with enhanced survival and poor prognosis.
Therapeutically, CD49d is a validated target. Monoclonal antibodies such as natalizumab block α4 integrins to reduce immune cell migration, providing clinical benefit in multiple sclerosis and Crohn’s disease. Ongoing strategies aim to refine targeting while minimizing immunosuppression-related risks.
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