GMFβ Antibody [C17A8] | Primary Antibodies

Application: Reactivity: Human, Pig

Lane 1: Mouse brain, Lane 2: Rat brain

Usage Information

Dilution
WB1:1000-1:8000 IHC1:50-1:500 IF1:200-1:800

Application
WB, IHC, IF, ELISA

Reactivity
Human, Pig

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
17 kDa 17 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
GMFβ Antibody [C17A8] detects endogenous levels of total GMFβ protein.

Clone
C17A8

Synonym(s)
Glia maturation factor beta; GMF-beta; GMFB

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.

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.

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

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

Tech Support

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

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%