Evidence map›Paper›PMID 16123801›Full record

ReviewOncogene2005

The role of Smad signaling in hematopoiesis.

Jonas Larsson, Stefan Karlsson

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed.

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6 more citing papers are in PubMed but not listed here.

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

2 authors.

Jonas LarssonMolecular Medicine and Gene Therapy, Institute of Laboratory Medicine, The Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund University, BMC A12, Lund 221 84, Sweden.
Stefan Karlsson

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TGF-beta family of ligands, including TGF-beta, bone morphogenetic protein (BMP) and activin, signal through Smad pathways to regulate the fate of hematopoietic progenitor and stem cells during development and postnatally. BMP regulates hematopoietic stem cell (HSC) specification during development, while TGF-beta1, 2 and 3 are not essential for the generation of HSCs. BMP4 can increase proliferation of human hematopoietic progenitors, while TGF-beta acts as a negative regulator of hematopoietic progenitor and stem cells in vitro. In contrast, TGF-beta signaling deficiency in vivo does not affect proliferation of HSCs and does not affect lineage choice either. Therefore, the outcome of Smad signaling is very context dependent in hematopoiesis and regulation of hematopoietic stem and progenitor cells is more complicated in the bone marrow microenvironment in vivo than is seen in liquid cultures ex vivo. Smad signaling regulates hematopoiesis by crosstalk with other regulatory signals and future research will define in more detail how the various pathways interact and how the knowledge obtained can be used to develop advanced cell therapies.

Indexed as

HematopoiesisAnimalsBone Marrow TransplantationBone Morphogenetic Protein 4Bone Morphogenetic ProteinsDNA-Binding ProteinsHematopoietic Stem CellsHumansSignal TransductionSmad ProteinsTrans-ActivatorsTransforming Growth Factor betaTransforming Growth Factor beta1BMP4 protein, humanBone Morphogenetic Protein 4Bone Morphogenetic ProteinsDNA-Binding ProteinsSmad ProteinsTGFB1 protein, humanTrans-ActivatorsTransforming Growth Factor betaTransforming Growth Factor beta1

Identifiers

PMID16123801

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.