ReviewBiology of the cell2015
Left-right asymmetry in the light of TOR: An update on what we know so far.
Review in Biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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
11 citing papers in PubMed.
- Bi-allelic KICS2 mutations impair KICSTOR complex-mediated mTORC1 regulation, causing intellectual disability and epilepsy.American journal of human genetics · 2025Article
- Cilia defects upon loss of WDR4 are linked to proteasomal hyperactivity and ubiquitin shortage.Cell death & disease · 2024Article
- Functions of cilia in cardiac development and disease.Annals of human genetics · 2024Review
- Cholesterol and Phosphoinositides in Cilia Biology.Advances in experimental medicine and biology · 2023Review
- Imbalanced mitochondrial function provokes heterotaxy via aberrant ciliogenesis.The Journal of clinical investigation · 2019Article
- Resting cells rely on the DNA helicase component MCM2 to build cilia.Nucleic acids research · 2019Article
- Pharmacological cholesterol depletion disturbs ciliogenesis and ciliary function in developing zebrafish.Communications biology · 2019Article
- Cell chirality regulates intercellular junctions and endothelial permeability.Science advances · 2018Article
- Cell volume changes contribute to epithelial morphogenesis in zebrafish Kupffer's vesicle.eLife · 2018Article
- Heterotaxy syndrome with intestinal malrotation, polysplenia and azygos continuity.Clinics and practice · 2018Article
- The analysis of heterotaxy patients reveals new loss-of-function variants of GRK5.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The internal left-right (LR) asymmetry is a characteristic that exists throughout the animal kingdom from roundworms over flies and fish to mammals. Cilia, which are antenna-like structures protruding into the extracellular space, are involved in establishing LR asymmetry during early development. Humans who suffer from dysfunctional cilia often develop conditions such as heterotaxy, where internal organs appear to be placed randomly. As a consequence to this failure in asymmetry development, serious complications such as congenital heart defects (CHD) occur. The mammalian (or mechanistic) target of rapamycin (mTOR) pathway has recently emerged as an important regulator regarding symmetry breaking. The mTOR pathway governs fundamental processes such as protein translation or metabolism. Its activity can be transduced by two complexes, which are called TORC1 and TORC2, respectively. So far, only TORC1 has been implicated with asymmetry development and appears to require very precise regulation. A number of recent papers provided evidence that dysregulated TORC1 results in alterations of motile cilia and asymmetry defects. In here, we give an update on what we know so far of mTORC1 in LR asymmetry development.
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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.