ArticleThe EMBO journal2001
A novel clathrin homolog that co-distributes with cytoskeletal components functions in the trans-Golgi network.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 67 citations in OpenAlex.
- DNAJC13 localization to endosomes is opposed by its J domain and its disordered C-terminus.Molecular biology of the cell · 2025Article
- Leveraging diverse cell death patterns in osteosarcoma patients and identification of the function of FADS2 in osteosarcoma cells.Scientific reports · 2025Article
- DNAJC13 localization to endosomes is opposed by its J domain and its disordered C-terminal tail.bioRxiv : the preprint server for biology · 2024Article
- CHC22 clathrin recruitment to the early secretory pathway requires two-site interaction with SNX5 and p115.The EMBO journal · 2024Article
- Mechanistic divergences of endocytic clathrin-coated vesicle formation in mammals, yeasts and plants.Journal of cell science · 2024Review
- CHC22 clathrin mediates traffic from early secretory compartments for human GLUT4 pathway biogenesis.The Journal of cell biology · 2020Article
- Coatopathies: Genetic Disorders of Protein Coats.Annual review of cell and developmental biology · 2019Review
- Article
- Taming the Triskelion: Bacterial Manipulation of Clathrin.Microbiology and molecular biology reviews : MMBR · 2019Review
- Interaction between autophagic vesicles and the Coxiella-containing vacuole requires CLTC (clathrin heavy chain).Autophagy · 2018Article
- CHC22 and CHC17 clathrins have distinct biochemical properties and display differential regulation and function.The Journal of biological chemistry · 2017Article
- Sequencing study on familial lung squamous cancer.Oncology letters · 2015Article
- A novel disorder reveals clathrin heavy chain-22 is essential for human pain and touch development.Brain : a journal of neurology · 2015Article
- Unconventional functions for clathrin, ESCRTs, and other endocytic regulators in the cytoskeleton, cell cycle, nucleus, and beyond: links to human disease.Cold Spring Harbor perspectives in biology · 2014Review
- Chemical-genetic disruption of clathrin function spares adaptor complex 3-dependent endosome vesicle biogenesis.Molecular biology of the cell · 2013Article
- Nuclear localization of clathrin involves a labile helix outside the trimerization domain.FEBS letters · 2013Article
- The CHC22 clathrin-GLUT4 transport pathway contributes to skeletal muscle regeneration.PloS one · 2013Article
- Clathrin promotes centrosome integrity in early mitosis through stabilization of centrosomal ch-TOG.The Journal of cell biology · 2012Article
- Down-regulation of ANAPC13 and CLTCL1: Early Events in the Progression of Preinvasive Ductal Carcinoma of the Breast.Translational oncology · 2012Article
- GCC185 plays independent roles in Golgi structure maintenance and AP-1-mediated vesicle tethering.The Journal of cell biology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
A clathrin homolog encoded on human chromosome 22 (CHC22) displays distinct biochemistry, distribution and function compared with conventional clathrin heavy chain (CHC17), encoded on chromosome 17. CHC22 protein is upregulated during myoblast differentiation into myotubes and is expressed at high levels in muscle and at low levels in non-muscle cells, relative to CHC17. The trimeric CHC22 protein does not interact with clathrin heavy chain subunits nor bind significantly to clathrin light chains. CHC22 associates with the AP1 and AP3 adaptor complexes but not with AP2. In non-muscle cells, CHC22 localizes to perinuclear vesicular structures, the majority of which are not clathrin coated. Treatments that disrupt the actin-myosin cytoskeleton or affect sorting in the trans-Golgi network (TGN) cause CHC22 redistribution. Overexpression of a subdomain of CHC22 induces altered distribution of TGN markers. Together these results implicate CHC22 in TGN membrane traffic involving the cytoskeleton.
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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.