ArticlePloS one2011
SIMPLE/LITAF expression induces the translocation of the ubiquitin ligase itch towards the lysosomal compartments.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Identification and Screening of LITAF Family Key Genes Responsive to Plant Secondary Metabolites inBiology · 2026Article
- Hsp70-Bag3 Module Regulates Macrophage Motility and Tumor Infiltration via Transcription Factor LITAF and CSF1.Cancers · 2022Article
- Endosomal recycling tubule scission and integrin recycling involve the membrane curvature-supporting protein LITAF.Journal of cell science · 2021Article
- The endosomal trafficking regulator LITAF controls the cardiac Nav1.5 channel via the ubiquitin ligase NEDD4-2.The Journal of biological chemistry · 2020Article
- A dysfunctional endolysosomal pathway common to two sub-types of demyelinating Charcot-Marie-Tooth disease.Acta neuropathologica communications · 2020Article
- LITAF (Lipopolysaccharide-Induced Tumor Necrosis Factor) Regulates Cardiac L-Type Calcium Channels by Modulating NEDD (Neural Precursor Cell Expressed Developmentally Downregulated Protein) 4-1 Ubiquitin Ligase.Circulation. Genomic and precision medicine · 2019Article
- PPAR δ inhibition protects against palmitic acid-LPS induced lipidosis and injury in cultured hepatocyte L02 cell.International journal of medical sciences · 2019Article
- VOPP1 promotes breast tumorigenesis by interacting with the tumor suppressor WWOX.BMC biology · 2018Article
- Article
- The topology, structure and PE interaction of LITAF underpin a Charcot-Marie-Tooth disease type 1C.BMC biology · 2016Article
- The Charcot Marie Tooth disease protein LITAF is a zinc-binding monotopic membrane protein.The Biochemical journal · 2016Article
- LPS-induced TNF-α factor mediates pro-inflammatory and pro-fibrogenic pattern in non-alcoholic fatty liver disease.Oncotarget · 2015Article
- Dysregulated Inflammatory Signaling upon Charcot-Marie-Tooth Type 1C Mutation of SIMPLE Protein.Molecular and cellular biology · 2015Article
- Article
- Mutation of SIMPLE in Charcot-Marie-Tooth 1C alters production of exosomes.Molecular biology of the cell · 2013Article
- Cellular LITAF interacts with frog virus 3 75L protein and alters its subcellular localization.Journal of virology · 2013Article
- Charcot-Marie-Tooth disease and intracellular traffic.Progress in neurobiology · 2012Review
- Accumulation of endogenous LITAF in aggresomes.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LITAF is a small cellular protein with an unknown function. The C-terminus of LITAF contains a highly conserved domain termed the SIMPLE-like domain (SLD), while the N-terminus contains two PPXY motifs that mediate protein-protein interactions with WW-domain containing proteins. LITAF also harbors two endosome/lysosome targeting sequences at its C-terminus, but there has been conflicting reports regarding its intracellular localization. Here, we demonstrate that LITAF is localized to the late endosome/lysosomal compartment in a variety of cell lines. We also show that Itch, a WW-domain containing protein, and LITAF strongly interact and that this interaction depends on the two PPXY motifs in the N-terminus of LITAF. Interestingly, co-expression of LITAF with Itch induces major changes in Itch intracellular localization, bringing Itch from the trans-Golgi network to lysosomes. We show that this re-localization is dependent upon the interaction with the PPXY sequences of LITAF, since disruption of these binding motifs completely abrogates Itch re-localization.
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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.