Evidence map›Paper›PMID 20023168›Full record

ArticleDevelopment (Cambridge, England)2010

Evidence for a role of vertebrate Disp1 in long-range Shh signaling.

L Alton Etheridge, T Quinn Crawford, Shile Zhang, Henk Roelink

Abstract read
In one paragraph

Article in Development (Cambridge, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
–field-weighted citation impact
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

36 citing papers in PubMed.

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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

4 authors.

L Alton EtheridgeDepartment of Molecular and Cell Biology, University of California at Berkeley, 16 Barker Hall #3204, Berkeley, CA 94720-3204, USA.
T Quinn Crawford
Shile Zhang
Henk Roelink

Funding

NICHD NIH HHS 1R01HD042307
6 · The paper itself

Abstract

Dispatched 1 (Disp1) encodes a twelve transmembrane domain protein that is required for long-range sonic hedgehog (Shh) signaling. Inhibition of Disp1 function, both by RNAi or dominant-negative constructs, prevents secretion and results in the accumulation of Shh in source cells. Measuring the Shh response in neuralized embryoid bodies (EBs) derived from embryonic stem (ES) cells, with or without Disp1 function, demonstrates an additional role for Disp1 in cells transporting Shh. Co-cultures with Shh-expressing cells revealed a significant reduction in the range of the contact-dependent Shh response in Disp1(-/-) neuralized EBs. These observations support a dual role for Disp1, not only in the secretion of Shh from the source cells, but also in the subsequent transport of Shh through tissue.

Indexed as

Signal TransductionAnimalsBlotting, WesternCell LineCells, CulturedDogsEmbryonic Stem CellsHedgehog ProteinsHumansMembrane ProteinsMiceRatsRNA InterferenceVertebratesHedgehog ProteinsMembrane Proteins

Identifiers

PMID20023168
PMCPMC2796928

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.