ArticleBiochemistry2009
The role of calcium in lipoprotein release by the low-density lipoprotein receptor.
Article in Biochemistry, 2009. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- The Cryo-EM structure of human CD163 bound to haptoglobin-hemoglobin reveals molecular mechanisms of hemoglobin scavenging.Nature communications · 2024Article
- Endosome rupture enables enteroviruses from the family Picornaviridae to infect cells.Communications biology · 2024Article
- CaAdvances in experimental medicine and biology · 2023Article
- Article
- Multivalent ions and biomolecules: Attempting a comprehensive perspective.Chemphyschem : a European journal of chemical physics and physical chemistry · 2020Review
- Article
- Vascular defects ofDisease models & mechanisms · 2019Article
- Identification of roles for H264, H306, H439, and H635 in acid-dependent lipoprotein release by the LDL receptor.Journal of lipid research · 2017Article
- Studies of the autoinhibitory segment comprising residues 31-60 of the prodomain of PCSK9: Possible implications for the mechanism underlying gain-of-function mutations.Molecular genetics and metabolism reports · 2016Article
- Release of Vesicular Stomatitis Virus Spike Protein G-Pseudotyped Lentivirus from the Host Cell Is Impaired upon Low-Density Lipoprotein Receptor Overexpression.Journal of virology · 2015Article
- PCSK9-mediated degradation of the LDL receptor generates a 17 kDa C-terminal LDL receptor fragment.Journal of lipid research · 2013Article
- LDL receptor and its family members serve as the cellular receptors for vesicular stomatitis virus.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Quantitative fluorescence imaging reveals point of release for lipoproteins during LDLR-dependent uptake.Journal of lipid research · 2013Article
- Mechanisms and concepts paving the way towards a complete transport cycle of plant vacuolar sorting receptors.The Plant cell · 2012Review
- The structure, dynamics, and binding of the LA45 module pair of the low-density lipoprotein receptor suggest an important role for LA4 in ligand release.Biochemistry · 2011Article
- Mechanisms and genetic determinants regulating sterol absorption, circulating LDL levels, and sterol elimination: implications for classification and disease risk.Journal of lipid research · 2011Review
- Role of an intramolecular contact on lipoprotein uptake by the LDL receptor.Biochimica et biophysica acta · 2011Article
- Apolipoprotein E: from lipid transport to neurobiology.Progress in lipid research · 2011Review
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 at 1 institution in 1 country.
Funding
Abstract
The LDL receptor (LDLR) mediates efficient endocytosis of VLDL, VLDL remnants, and LDL. As part of the uptake process, the LDLR releases lipoproteins in endosomes. Released lipoproteins are subsequently trafficked to lysosomes for degradation, while the LDLR recycles back to the cell surface for further rounds of uptake. Endosomes have at least two features that can promote lipoprotein release: an acidic pH and low concentrations of free calcium. The relative contributions of acidic pH and low free calcium to lipoprotein release are not known. Here, we generated fibroblasts that express either normal LDLR or an LDLR variant that is unable to employ the acid-dependent release mechanism to determine the relative contributions of acidic pH and low free calcium on lipoprotein release. We show that endosomal concentrations of free calcium can drive lipoprotein release at rates that are similar to those of acid-dependent release and that the calcium-dependent and acid-dependent mechanisms can cooperate during lipoprotein release. Assessment of lipoprotein uptake by these two cell lines showed that LDL uptake requires the acid-dependent mechanism, while uptake of the VLDL remnant, beta-VLDL, does not. We propose that endosomes use both the acid-dependent and calcium-dependent release mechanisms to drive lipoprotein release and that the acid-dependent process is only required for LDL release.
Indexed as
Identifiers
What OpenQuestion holds
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.