Evidence map›Paper›PMID 20870970›Full record

ArticleDiabetes2011

Targeted inactivation of kinesin-1 in pancreatic β-cells in vivo leads to insulin secretory deficiency.

Ju Cui, Zai Wang, Qianni Cheng, Raozhou Lin, Xin-Mei Zhang, Po Sing Leung, Neal G Copeland, Nancy A Jenkins, Kwok-Ming Yao, Jian-Dong Huang

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 66 citations in OpenAlex.

  1. Roles of molecular motors in insulin-secreting beta cells.Current opinion in cell biology · 2025
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  8. Regulation of insulin secretion by the post-translational modifications.Frontiers in cell and developmental biology · 2023
    Review
  9. Article
  10. Insulin granule biogenesis and exocytosis.Cellular and molecular life sciences : CMLS · 2021
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  11. Review
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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

10 authors at 4 institutions in 3 countries.

Ju CuiDepartment of Biochemistry, The University of Hong Kong, Hong Kong.
Zai Wang
Qianni Cheng
Raozhou Lin
Xin-Mei Zhang
Po Sing Leung
Neal G Copeland
Nancy A Jenkins
Kwok-Ming Yao
Jian-Dong Huang
Chinese University of Hong Kong · CNUniversity of Hong Kong · HKAgency for Science, Technology and Research · SGInstitute of Molecular and Cell Biology · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSuppression of Kinesin-1 by antisense oligonucleotides, or overexpression of dominant-negative acting kinesin heavy chain, has been reported to affect the sustained phase of glucose-stimulated insulin secretion in β-cells in vitro. In this study, we examined the in vivo physiological role of Kinesin-1 in β-cell development and function. RESEARCH DESIGN AND

methodsA Cre-LoxP strategy was used to generate conditional knockout mice in which the Kif5b gene is specifically inactivated in pancreatic β-cells. Physiological and histological analyses were carried out in Kif5b knockout mice as well as littermate controls.

resultsMice with β-cell specific deletion of Kif5b (Kif5b(fl/)⁻:RIP2-Cre) displayed significantly retarded growth as well as slight hyperglycemia in both nonfasting and 16-h fasting conditions compared with control littermates. In addition, Kif5b(fl/)⁻:RIP2-Cre mice displayed significant glucose intolerance, which was not due to insulin resistance but was related to an insulin secretory defect in response to glucose challenge. These defects of β-cell function in mutant mice were not coupled with observable changes in islet morphology, islet cell composition, or β-cell size. However, compared with controls, pancreas of Kif5b(fl/)⁻:RIP2-Cre mice exhibited both reduced islet size and increased islet number, concomitant with an increased insulin vesicle density in β-cells.

conclusionsIn addition to being essential for maintaining glucose homeostasis and regulating β-cell function, Kif5b may be involved in β-cell development by regulating β-cell proliferation and insulin vesicle synthesis.

Indexed as

Amino Acid SequenceAnimalsBase SequenceBlotting, WesternDNA PrimersEnzyme-Linked Immunosorbent AssayGenotypeHumansInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansKinesinsMaleMiceMice, KnockoutDNA PrimersInsulinKIF11 protein, humanKif5b protein, mouseKinesinsOligonucleotides, AntisensePeptide Fragments

Identifiers

PMID20870970
PMCPMC3012189
OpenAlexW2170512365

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.