Evidence map›Paper›PMID 33179593›Full record

ArticleeLife2020

BLOS1 mediates kinesin switch during endosomal recycling of LDL receptor.

Chang Zhang, Chanjuan Hao, Guanghou Shui, Wei Li

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 29% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. BLOC1S1 Attenuates B. Melitensis 16M LPS-Triggered Autophagy by Spatial Confinement of TDP-43.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  2. Review
  3. Article
  4. Article
  5. Regulation ofMolecular biology of the cell · 2022
    Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Chang ZhangState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.ORCID 0000-0002-3930-9799
Chanjuan HaoBeijing Key Laboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Guanghou ShuiState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Wei LiBeijing Key Laboratory for Genetics of Birth Defects, Beijing Pediatric Research Institute; MOE Key Laboratory of Major Diseases in Children; Genetics and Birth Defects Control Center, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.ORCID 0000-0002-0248-5510
Capital Medical University · CNChinese Academy of Sciences · CN

Funding

Chinese Academy of Sciences XDA12030211Ministry of Science and Technology of the People's Republic of China 2019YFA0802104National Natural Science Foundation of China 31830054National Natural Science Foundation of China 81670789National Natural Science Foundation of China 91539204National Natural Science Foundation of China 91954104
6 · The paper itself

Abstract

Low-density lipoprotein receptor (LDLR) in hepatocytes plays a key role in plasma clearance of circulating LDL and in whole body cholesterol homeostasis. The trafficking of LDLR is highly regulated in clathrin-dependent endocytosis, endosomal recycling and lysosomal degradation. Current studies focus on its endocytosis and degradation. However, the detailed molecular and cellular mechanisms underlying its endosomal recycling are largely unknown. We found that BLOS1, a shared subunit of BLOC-1 and BORC, is involved in LDLR endosomal recycling. Loss of BLOS1 leads to less membrane LDLR and impairs LDL clearance from plasma in hepatocyte-specific BLOS1 knockout mice. BLOS1 interacts with kinesin-3 motor KIF13A, and BLOS1 acts as a new adaptor for kinesin-2 motor KIF3 to coordinate kinesin-3 and kinesin-2 during the long-range transport of recycling endosomes (REs) to plasma membrane along microtubule tracks to overcome hurdles at microtubule intersections. This provides new insights into RE's anterograde transport and the pathogenesis of dyslipidemia.

Indexed as

AnimalsCarrier ProteinsGene Expression RegulationHepatocytesHep G2 CellsHumansIntracellular Signaling Peptides and ProteinsKinesinsMiceMitochondrial ProteinsNerve Tissue ProteinsReceptors, LDLSingle-Cell AnalysisBLOC1S1 protein, mouseCarrier ProteinsIntracellular Signaling Peptides and ProteinsKinesinsKxd1 protein, mouseMitochondrial ProteinsNerve Tissue ProteinsReceptors, LDLBLOS1cell biologydyslipidemiaendosomal recyclingkinesinsLDL receptormicrotubulesmouse

Identifiers

PMID33179593
PMCPMC7688313
OpenAlexW3104982114

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.