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Description
GMF-β Protein, MouseProduct Specification Species Mouse Synonyms Glia maturation factor beta, GMF beta Accession Q9CQI3 Amino Acid Sequence Ser2 His142 Expression System E. coli Molecular Weight 16 kDa (Reducing) Purity >95% by SDS PAGE and HPLC Endotoxin <0. 1EU g Conjugation Unconjugated Tag No Tag Physical Appearance Lyophilized powder Storage Buffer PBS, pH7. 4 Reconstitution Reconstitute at 0. 1 1 mg ml according to the size in ultrapure water after rapid
Product Specification
| Species | Mouse |
| Synonyms | Glia maturation factor beta, GMF-beta |
| Accession | Q9CQI3 |
| Amino Acid Sequence | Ser2-His142 |
| Expression System | E.coli |
| Molecular Weight | 16 kDa (Reducing) |
| Purity | >95% by SDS-PAGE and HPLC |
| Endotoxin | <0.1EU/μg |
| Conjugation | Unconjugated |
| Tag | No Tag |
| Physical Appearance | Lyophilized powder |
| Storage Buffer | PBS, pH7.4 |
| Reconstitution | Reconstitute at 0.1-1 mg/ml according to the size in ultrapure water after rapid centrifugation. |
| Stability & Storage | ·12 months from date of receipt, lyophilized powder stored at -20 to -80℃. |
| Reference | Trends Cell Biol. 2018 Sep;28(9):749-760. |
Background
Glia maturation factor-β (GMF-β) is a highly evolutionarily conserved protein belonging to the ADF/cofilin superfamily, first isolated from bovine brain tissue in 1972. Predominantly expressed in the central nervous system (CNS), GMF-β is also detected in various peripheral tissues including colon, thymus, and kidney. As a critical regulator of the Arp2/3 complex-mediated actin cytoskeleton remodeling, GMF-β controls branched actin content, lamellipodial dynamics, and cellular motility. Structurally, GMF-β lacks a classical signal peptide but can be secreted through non-conventional pathways, functioning as both an intracellular signaling molecule and an extracellular modulator of glial cell maturation and differentiation. Whole-body knockout studies in mice demonstrate that GMF-β deficiency is non-lethal, suggesting potential redundancy or compensation mechanisms, yet reveals marked impairments in motor performance, learning capabilities, and inflammatory responses.
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