Evidence map›Paper›PMID 16554367›Full record

ArticleMolecular biology of the cell2006

The kinesin KIF1C and microtubule plus ends regulate podosome dynamics in macrophages.

Petra Kopp, Reiner Lammers, Martin Aepfelbacher, Günther Woehlke, Thomas Rudel, Nikolaus Machuy, Walter Steffen, Stefan Linder

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

59 citing papers in PubMed, 133 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Petra KoppInstitut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Ludwig-Maximilians-Universität, 80336 Munich, Germany.
Reiner Lammers
Martin Aepfelbacher
Günther Woehlke
Thomas Rudel
Nikolaus Machuy
Walter Steffen
Stefan Linder
Ludwig-Maximilians-Universität München · DEMax Planck Society · DEMedizinische Hochschule Hannover · DEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microtubules are important for the turnover of podosomes, dynamic, actin-rich adhesions implicated in migration and invasion of monocytic cells. The molecular basis for this functional dependency, however, remained unclear. Here, we show that contact by microtubule plus ends critically influences the cellular fate of podosomes in primary human macrophages. In particular, we identify the kinesin KIF1C, a member of the Kinesin-3 family, as a plus-end-enriched motor that targets regions of podosome turnover. Expression of mutation constructs or small interfering RNA-/short hairpin RNA-based depletion of KIF1C resulted in decreased podosome dynamics and ultimately in podosome deficiency. Importantly, protein interaction studies showed that KIF1C binds to nonmuscle myosin IIA via its PTPD-binding domain, thus providing an interface between the actin and tubulin cytoskeletons, which may facilitate the subcellular targeting of podosomes by microtubules. This is the first report to implicate a kinesin in podosome regulation and also the first to describe a function for KIF1C in human cells.

Indexed as

Cell DifferentiationCell Membrane StructuresCells, CulturedCloning, MolecularEscherichia coliHumansKinesinsMacrophagesMicroinjectionsMicrotubulesMutagenesisPlasmidsReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingTransfectionKIF1C protein, humanKinesinsRNA, Small Interfering

Identifiers

PMID16554367
PMCPMC1474789
OpenAlexW2111139783

What OpenQuestion holds

Textmetadata
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.