ArticleMolecular biology of the cell2007
Avl9p, a member of a novel protein superfamily, functions in the late secretory pathway.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Avl9 defines a family of DENN domain GTPase-activating proteins.The Journal of cell biology · 2026Article
- TCOF1 affects Golgi secretory pathway contributing to the angiogenesis in renal cancer.Cell communication and signaling : CCS · 2026Article
- Avl9 defines a family of GTPase-activating proteins that regulate diverse cell biological functions.bioRxiv : the preprint server for biology · 2026Article
- Circular RNA in Non-small Cell Lung Carcinoma: Identification of Targets and New Treatment Modalities.Cancer genomics & proteomics · 2023Review
- Osh-dependent and -independent Regulation of PI4P Levels During Polarized Growth ofMolecular biology of the cell · 2023Article
- High-resolution secretory timeline from vesicle formation at the Golgi to fusion at the plasma membrane ineLife · 2022Article
- The Fungal Protein Mes1 Is Required for Morphogenesis and Virulence in the Dimorphic PhytopathogenJournal of fungi (Basel, Switzerland) · 2022Article
- AVL9 promotes colorectal carcinoma cell migration via regulating EGFR expression.Biological procedures online · 2022Article
- hsa_circ_0058357 acts as a ceRNA to promote non‑small cell lung cancer progression via the hsa‑miR‑24‑3p/AVL9 axis.Molecular medicine reports · 2021Article
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- Hypoxia-regulated lncRNA CRPAT4 promotes cell migration via regulating AVL9 in clear cell renal cell carcinomas.OncoTargets and therapy · 2018Article
- DENND2B activates Rab13 at the leading edge of migrating cells and promotes metastatic behavior.The Journal of cell biology · 2015Article
- Cancer driver-passenger distinction via sporadic human and dog cancer comparison: a proof-of-principle study with colorectal cancer.Oncogene · 2014Article
- Cancer driver candidate genes AVL9, DENND5A and NUPL1 contribute to MDCK cystogenesis.Oncoscience · 2014Article
- Actin acting at the Golgi.Histochemistry and cell biology · 2013Review
- The synaptobrevin homologue Snc2p recruits the exocyst to secretory vesicles by binding to Sec6p.The Journal of cell biology · 2013Article
- A conserved regulatory mode in exocytic membrane fusion revealed by Mso1p membrane interactions.Molecular biology of the cell · 2013Article
- Crystal structure of folliculin reveals a hidDENN function in genetically inherited renal cancer.Open biology · 2012Article
- Rab14 and its exchange factor FAM116 link endocytic recycling and adherens junction stability in migrating cells.Developmental cell · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The branching of exocytic transport routes in both yeast and mammalian cells has complicated studies of the late secretory pathway, and the mechanisms involved in exocytic cargo sorting and exit from the Golgi and endosomes are not well understood. Because cargo can be sorted away from a blocked route and secreted by an alternate route, mutants defective in only one route do not exhibit a strong secretory phenotype and are therefore difficult to isolate. In a genetic screen designed to isolate such mutants, we identified a novel conserved protein, Avl9p, the absence of which conferred lethality in a vps1Delta apl2Delta strain background (lacking a dynamin and an adaptor-protein complex 1 subunit). Depletion of Avl9p in this strain resulted in secretory defects as well as accumulation of Golgi-like membranes. The triple mutant also had a depolarized actin cytoskeleton and defects in polarized secretion. Overexpression of Avl9p in wild-type cells resulted in vesicle accumulation and a post-Golgi defect in secretion. Phylogenetic analysis indicated evolutionary relationships between Avl9p and regulators of membrane traffic and actin function.
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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.