Datasheet

生物学的記述

Specificity	GMFβ Antibody [C17A8] detects endogenous levels of total GMFβ protein.
Background	GMFβ (glia maturation factor beta), a small actin-binding protein predominantly expressed in astrocytes and select neurons of the central nervous system, functions as a growth and differentiation factor that orchestrates glial activation and neuronal remodeling during development and injury response. It adopts a compact actin-depolymerizing fold similar to ADF-H cofilin family members, enabling direct interaction with G-actin to promote disassembly of F-actin filaments at the pointed ends. The core mechanism involves GMFβ disrupting Arp2/3-mediated branched networks in reactive astrocytes, which destabilizes lamellipodia to favor filopodial extensions while activating Rac1-Cdc42 signaling for process elongation; concurrently, it upregulates neurotrophins like BDNF and NGF transcription through Smad1/5-STAT3 pathways, fostering neurite outgrowth and synaptic plasticity in co-cultured neurons. This dual action integrates into the NF-κB inflammatory cascade where GMFβ amplifies IL-6, TNF-α, and GM-CSF release from microglia via PKA phosphorylation, sustaining reactive gliosis while counteracting Aβ-induced cytotoxicity through iNOS modulation and UCP2/4 downregulation for mitochondrial ROS management. GMFβ drives Bergmann glia differentiation in cerebellum and Müller cell maturation in retina, positioning it as a key mediator of CNS repair that researchers exploit in organotypic slice cultures to dissect astrocyte-neuron crosstalk or track differentiation kinetics via phospho-specific probes. Upregulation characterizes Alzheimer's disease progression with enhanced glial scarring, while deficiency impairs recovery from cryogenic lesions. Its SUMOylation at multiple sites enhances nuclear translocation for cytokine gene induction.

Specificity

GMFβ Antibody [C17A8] detects endogenous levels of total GMFβ protein.

Background

GMFβ (glia maturation factor beta), a small actin-binding protein predominantly expressed in astrocytes and select neurons of the central nervous system, functions as a growth and differentiation factor that orchestrates glial activation and neuronal remodeling during development and injury response. It adopts a compact actin-depolymerizing fold similar to ADF-H cofilin family members, enabling direct interaction with G-actin to promote disassembly of F-actin filaments at the pointed ends. The core mechanism involves GMFβ disrupting Arp2/3-mediated branched networks in reactive astrocytes, which destabilizes lamellipodia to favor filopodial extensions while activating Rac1-Cdc42 signaling for process elongation; concurrently, it upregulates neurotrophins like BDNF and NGF transcription through Smad1/5-STAT3 pathways, fostering neurite outgrowth and synaptic plasticity in co-cultured neurons. This dual action integrates into the NF-κB inflammatory cascade where GMFβ amplifies IL-6, TNF-α, and GM-CSF release from microglia via PKA phosphorylation, sustaining reactive gliosis while counteracting Aβ-induced cytotoxicity through iNOS modulation and UCP2/4 downregulation for mitochondrial ROS management. GMFβ drives Bergmann glia differentiation in cerebellum and Müller cell maturation in retina, positioning it as a key mediator of CNS repair that researchers exploit in organotypic slice cultures to dissect astrocyte-neuron crosstalk or track differentiation kinetics via phospho-specific probes. Upregulation characterizes Alzheimer's disease progression with enhanced glial scarring, while deficiency impairs recovery from cryogenic lesions. Its SUMOylation at multiple sites enhances nuclear translocation for cytokine gene induction.

使用情報

Application

WB, IHC, IF, ELISA

Dilution

WB	IHC	IF
1:1000-1:8000	1:50-1:500	1:200-1:800

Reactivity

Human, Pig

Source

Mouse Monoclonal Antibody

MW

17 kDa

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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/29445286/
https://pubmed.ncbi.nlm.nih.gov/18395194/

Application Data

WB

Validated by Selleck

Lane 1: Mouse brain, Lane 2: Rat brain