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Cat.No.: F4755
| Dilution |
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| Application |
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| WB, IHC |
| Reactivity |
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| Mouse |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW |
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| 60-100 kDa |
| Positive Control | GL261 syngeneic tumor; Mouse thymus; LL/2 syngeneic tumor; CT26 syngeneic tumor; Mouse spleen; Mouse small intestine; Mouse lung; Mouse CD8+ T cells; EL4 cells; BA/F3 cells |
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| Negative Control | Neuro-2a cells |
| Specificity |
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| CD62L/L-Selectin Antibody [H14P17] detects endogenous levels of total CD62L/L-Selectin protein. |
| Clone |
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| H14P17 |
| Synonym(s) |
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| L-selectin; CD62 antigen-like family member L; Leukocyte adhesion molecule 1 (LAM-1); LECAM1; Lymphocyte antigen 22; lY-22; Lymphocyte surface MEL-14 antigen; CD62L; Sell; Lnhr; Ly-22; Ly22 |
| Background |
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| CD62L (L-Selectin, SELL) is a type-I transmembrane glycoprotein belonging to the selectin family of cell adhesion molecules (alongside E- and P-selectin), expressed on most circulating leukocytes including naive T cells, central memory T cells, monocytes, and neutrophils, where it mediates initial tethering and rolling on high endothelial venules (HEVs) in lymphoid tissues via weak calcium-dependent bonds with sulfated O-linked glycans on GlyCAM-1, CD34, and MAdCAM-1. It comprises an N-terminal C-type lectin domain for ligand carbohydrate recognition (key residues like Ca²⁺-coordinating Asp/Asp/Glu in epidermal growth factor-like domain), a single EGF-like domain, two consensus repeats for rigidity, a highly basic 17-residue cytoplasmic tail interacting with ERM proteins (ezrin-radixin-moesin), calmodulin, and PKC for cytoskeletal linkage and signaling, and a membrane-proximal extracellular stalk cleaved by ADAM17 protease during activation. Its primary functions involve facilitating lymphocyte homing to lymph nodes by enabling shear-resistant rolling on HEVs, promoting monocyte protrusion and transendothelial migration (TEM) through ERM-mediated actin remodeling, and signaling via Src kinases/FAK to enhance chemotaxis toward CCL21; post-activation shedding of CD62L is antigen-specific, downregulating HEV binding while enabling front-back polarity, cytotoxic granule mobilization (CD107a+), and perforin/granzyme release in effector T cells. CD62L distinguishes naive/central memory (CD62L^hi) from effector memory (CD62L^lo) T cells, regulates inflammation by balancing recruitment and emigration, and supports immune surveillance; shedding-resistant mutants impair lytic function by ~50%, linking ectodomain release to cytoskeleton reorganization. Dysregulated CD62L shedding contributes to chronic lymphocytic leukemia infiltration, excessive inflammation in atherosclerosis, and impaired antiviral immunity. |
| References |
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