ArticleBioarchitecture
Filamin A and Big2: a shared endocytic pathway.
Article in Bioarchitecture. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Multiple genomic copy number variants associated with periventricular nodular heterotopia indicate extreme genetic heterogeneity.European journal of human genetics : EJHG · 2019Trial
- A conserved Arf-GEF modulates axonal integrity through RAB-35 by altering neuron-epidermal attachment.Journal of cell science · 2026Article
- ARFGEF2-Related Periventricular Nodular Heterotopia: A Case Report and Literature Review.NeuroSci · 2026Article
- Endoplasmic reticulum and Golgi stress in microcephaly.Cell stress · 2019Review
- Article
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1 author at 1 institution in 2 countries.
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Abstract
Neural proliferation, migration and differentiation require reorganization of the actin cytoskeleton and regulation of vesicle trafficking to provide stability in maintaining cell adhesions, allow for changes in cell shape, and establishing cell polarity. Human disorders involving the actin-binding Filamin A (FLNA) and vesicle trafficking Brefeldin-associated guanine exchange factor 2 (BIG2 is encoded by the ARFGEF2 gene) proteins are implicated in these various developmental processes, resulting in a malformation of cortical development called periventricular heterotopia (nodules along the ventricular lining) and microcephaly (small brain). Here we discuss several recent reports from our laboratory that demonstrate a shared role for both proteins in actin-associated vesicle trafficking, which is required to maintain the expression and stability of cell adhesion and cell cycle associated molecules during cortical development. While changes in FLNA and BIG2 have first been linked to disorders involving the central nervous system, increasing reports suggest they are associated with aberrant development of various other organ systems in the body. These studies suggest that vesicle trafficking defects in FLN-GEF dependent pathways may contribute to a much broader phenotype than previously realized.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.