E-Selectin / CD62E (SELE) Antibody (FITC)

Este producto es parte de SELE - selectin E
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689€ (100 tests)

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935106861
info@markelab.com
name
E-Selectin / CD62E (SELE) Antibody (FITC)
category
Primary Antibodies
provider
Abbexa
reference
abx413581
tested applications
FCM

Description

CD62 Antigen-Like Family Member E (CD62E) Antibody (FITC) is a Mouse Monoclonal antibody against CD62 Antigen-Like Family Member E (CD62E).

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
E-Selectin / CD62E (SELE)
Host
Mouse
Reactivity
Human
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Monoclonal
Conjugation
FITC
Isotype
IgG2a
Purification
Purified
Size 1
100 tests
Form
Liquid
Tested Applications
FCM
Buffer
Tris-buffered saline, 1% BSA. Contains sodium azide.
Availability
Shipped within 3-7 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
P16581
Alias
ELAM,ESEL,CD62E,ELAM1,LECAM2,selectin-e,E-selectin,CD62 antigen-like family member E,Endothelial leukocyte adhesion molecule 1,Leukocyte-endothelial cell adhesion molecule 2
Background
Antibody anti-SELE
Status
RUO

Descripción

Selectin E (SELE) is an adhesion molecule expressed on activated endothelial cells in response to inflammatory cytokines such as TNF-α and IL-1β, playing a pivotal role in the recruitment of leukocytes to sites of inflammation. It mediates the rolling and tethering of leukocytes on the endothelium by binding to specific glycoprotein ligands on the surface of leukocytes, such as PSGL-1, facilitating their migration into tissues. SELE is crucial in early-stage inflammatory responses and is involved in various pathophysiological processes, including atherosclerosis, autoimmune diseases, and cancer metastasis. Dysregulation of SELE expression has been associated with increased endothelial dysfunction and vascular inflammation, contributing to the development of cardiovascular diseases. Its expression is transient and tightly regulated by transcriptional mechanisms, ensuring that leukocyte recruitment occurs precisely during inflammatory responses. Therapeutic targeting of SELE has been explored to mitigate excessive inflammation, with strategies focusing on blocking its interaction with ligands to prevent leukocyte adhesion and infiltration. Additionally, SELE is being investigated as a biomarker for endothelial activation and vascular inflammation in conditions such as sepsis and chronic inflammatory disorders. Its role in mediating cell adhesion under shear stress highlights its importance in maintaining vascular integrity during immune surveillance and inflammatory responses.

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