Ezrin Antibody [L20P21] | Primary Antibodies

Application: Reactivity: Mouse, Human

Usage Information

Dilution
WB1:100 - 1:750 IHC1:2000 FCM1:2000

Application
WB, IHC, FCM

Reactivity
Mouse, Human

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
69 kDa 81 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

Specificity
Ezrin Antibody [L20P21] detects endogenous levels of total Ezrin protein.

Clone
L20P21

Synonym(s)
VIL2, EZR, Ezrin, Cytovillin, Villin-2, p81

Background
Ezrin is a member of the ERM (ezrin–radixin–moesin) family that functions as a membrane–cytoskeleton linker and signaling hub, localizing predominantly to the plasma membrane where it connects integral membrane proteins and phospholipids to cortical F‑actin to support cell shape, polarity, and motility. The protein is organized into an N‑terminal FERM domain that binds membrane partners and phosphatidylinositol‑4,5‑bisphosphate, a central α‑helical region, and a C‑terminal actin‑binding domain, and intramolecular association between the FERM and tail regions maintains an autoinhibited conformation that is released by PIP2 binding and phosphorylation at a conserved threonine, which exposes binding sites for adhesion molecules, scaffold proteins such as EBP50/NHERF1, and F‑actin. Active ezrin concentrates in microvilli, membrane ruffles, and other actin‑rich protrusions, where it stabilizes these structures and organizes complexes containing adhesion receptors, receptor tyrosine kinases, and G‑protein–coupled receptors, linking upstream cues to Rho family GTPase signaling and to downstream pathways including PI3K–AKT, MAPK/ERK, and NF‑κB that influence survival, proliferation, and migration. Ezrin interacts with and is regulated by kinases such as PKC and ROCK, and its phosphorylation status coordinates with Rho‑GTPase activity to control assembly and disassembly of cell–cell and cell–matrix contacts, turnover of focal adhesions, and directional motility during invasion and metastasis. High ezrin expression in osteosarcoma is associated with increased metastatic propensity, lung metastasis, and poor outcome, and in osteosarcoma models ezrin expression is required for metastatic outgrowth, with ezrin‑dependent activation of an AKT–mTOR–S6K1/4E‑BP1 axis that supports protein synthesis and metabolic adaptation in the lung microenvironment. Ezrin operates as a central coordinator of metastasis-related processes by linking the plasma membrane to the actin cytoskeleton, facilitating membrane trafficking, and organizing cytoskeletal remodeling. Ezrin also modulates intracellular signaling pathways and mediates interactions with immune and stromal cells in the tumor microenvironment, collectively promoting tumor cell migration, invasion, and metastatic dissemination.

Background

Ezrin is a member of the ERM (ezrin–radixin–moesin) family that functions as a membrane–cytoskeleton linker and signaling hub, localizing predominantly to the plasma membrane where it connects integral membrane proteins and phospholipids to cortical F‑actin to support cell shape, polarity, and motility. The protein is organized into an N‑terminal FERM domain that binds membrane partners and phosphatidylinositol‑4,5‑bisphosphate, a central α‑helical region, and a C‑terminal actin‑binding domain, and intramolecular association between the FERM and tail regions maintains an autoinhibited conformation that is released by PIP2 binding and phosphorylation at a conserved threonine, which exposes binding sites for adhesion molecules, scaffold proteins such as EBP50/NHERF1, and F‑actin. Active ezrin concentrates in microvilli, membrane ruffles, and other actin‑rich protrusions, where it stabilizes these structures and organizes complexes containing adhesion receptors, receptor tyrosine kinases, and G‑protein–coupled receptors, linking upstream cues to Rho family GTPase signaling and to downstream pathways including PI3K–AKT, MAPK/ERK, and NF‑κB that influence survival, proliferation, and migration. Ezrin interacts with and is regulated by kinases such as PKC and ROCK, and its phosphorylation status coordinates with Rho‑GTPase activity to control assembly and disassembly of cell–cell and cell–matrix contacts, turnover of focal adhesions, and directional motility during invasion and metastasis. High ezrin expression in osteosarcoma is associated with increased metastatic propensity, lung metastasis, and poor outcome, and in osteosarcoma models ezrin expression is required for metastatic outgrowth, with ezrin‑dependent activation of an AKT–mTOR–S6K1/4E‑BP1 axis that supports protein synthesis and metabolic adaptation in the lung microenvironment. Ezrin operates as a central coordinator of metastasis-related processes by linking the plasma membrane to the actin cytoskeleton, facilitating membrane trafficking, and organizing cytoskeletal remodeling. Ezrin also modulates intracellular signaling pathways and mediates interactions with immune and stromal cells in the tumor microenvironment, collectively promoting tumor cell migration, invasion, and metastatic dissemination.

References
https://pubmed.ncbi.nlm.nih.gov/37371090/ https://pubmed.ncbi.nlm.nih.gov/33240887/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%