pathway Info Card

Actin Filament Depolymerization

Information about Actin Filament Depolymerization: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.

Overview of Actin Filament Depolymerization

Most recent studies have shown that Actin Filament Depolymerization shares some biological mechanisms with cell-migration, cell-motility, complement-activation, cytokinesis, cytoplasm-organization, endocytosis, exocytosis, inflammatory-response, localization, muscle-contraction, phagocytosis, pollen-germination, pollen-tube-growth, protein-phosphorylation, protein-secretion, rna-transport, translation, transport, virulence.

Among the many pathways, these few ones have gauged particular interests from scientists studying Actin Filament Depolymerization, and have been seen in publications frequently: cell-migration, cell-motility, complement-activation, cytokinesis, cytoplasm-organization, endocytosis, exocytosis, inflammatory-response, localization, muscle-contraction, phagocytosis, pollen-germination, pollen-tube-growth, protein-phosphorylation, protein-secretion, rna-transport, translation, transport, virulence

Quite a number of genes have been found to play important roles in Actin Filament Depolymerization, such as ACTR2, CAP1, CFL1, CFL2, DNM2, DSTN, GJB2, GJB6, GSN, NPM1, PTGER4, RAB8A, SGSM3, TJP1, TWF1, TXN, VPS72, WAS. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.

In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this pathway. Plesae stay updated.

Actin Filament Depolymerization Related Genes

click to see detail information for each gene

ACTR2 CAP1 CFL1
CFL2 DNM2 DSTN
GJB2 GJB6 GSN
NPM1 PTGER4 RAB8A
SGSM3 TJP1 TWF1
TXN VPS72 WAS