Evidence map›Paper›PMID 19015308›Full record

ArticleThe Journal of experimental medicine2008

A point mutation in the murine Hem1 gene reveals an essential role for Hematopoietic protein 1 in lymphopoiesis and innate immunity.

Heon Park, Karen Staehling-Hampton, Mark W Appleby, Mary E Brunkow, Tania Habib, Yi Zhang, Fred Ramsdell, H Denny Liggitt, Brian Freie, Mark Tsang and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

39 citing papers in PubMed, 58 citations in OpenAlex.

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  16. Proteome Profiling of PMJ2-R and Primary Peritoneal Macrophages.International journal of molecular sciences · 2021
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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

14 authors at 3 institutions in 1 country.

Heon ParkDepartment of Comparative Medicine, University of Washington, Seattle, WA 98195, USA.
Karen Staehling-Hampton
Mark W Appleby
Mary E Brunkow
Tania Habib
Yi Zhang
Fred Ramsdell
H Denny Liggitt
Brian Freie
Mark Tsang
George Carlson
Sherree Friend
Charles Frevert
Brian M Iritani
University of Washington · USFred Hutch Cancer Center · USMcLaughlin Research Institute · US

Funding

Investigation of Myc Oncoprotein in B lymphocyte Development and TransformationK26RR024462 · NCRR · UNIVERSITY OF WASHINGTON · PI IRITANI, BRIAN M · 2008 to 2011
$446k
Investigation of Myc Oncoprotein in B lymphocyte Development and TransformationK26OD011060 · OD · UNIVERSITY OF WASHINGTON · PI IRITANI, BRIAN M · 2012 to 2012
$115k
NCRR NIH HHS K26 RR024462NIAID NIH HHS R01AI0535468NIH HHS K26 OD011060
6 · The paper itself

Abstract

Hem1 (Hematopoietic protein 1) is a hematopoietic cell-specific member of the Hem family of cytoplasmic adaptor proteins. Orthologues of Hem1 in Dictyostelium discoideum, Drosophila melanogaster, and Caenorhabditis elegans are essential for cytoskeletal reorganization, embryonic cell migration, and morphogenesis. However, the in vivo functions of mammalian Hem1 are not known. Using a chemical mutagenesis strategy in mice to identify novel genes involved in immune cell functions, we positionally cloned a nonsense mutation in the Hem1 gene. Hem1 deficiency results in defective F-actin polymerization and actin capping in lymphocytes and neutrophils caused by loss of the Rac-controlled actin-regulatory WAVE protein complex. T cell development is disrupted in Hem1-deficient mice at the CD4(-)CD8(-) (double negative) to CD4(+)CD8(+) (double positive) cell stages, whereas T cell activation and adhesion are impaired. Hem1-deficient neutrophils fail to migrate in response to chemotactic agents and are deficient in their ability to phagocytose bacteria. Remarkably, some Rac-dependent functions, such as Th1 differentiation and nuclear factor kappaB (NF-kappaB)-dependent transcription of proinflammatory cytokines proceed normally in Hem1-deficient mice, whereas the production of Th17 cells are enhanced. These results demonstrate that Hem1 is essential for hematopoietic cell development, function, and homeostasis by controlling a distinct pathway leading to cytoskeletal reorganization, whereas NF-kappaB-dependent transcription proceeds independently of Hem1 and F-actin polymerization.

Indexed as

Membrane ProteinsPoint MutationActinsAdaptor Proteins, Signal TransducingAnemiaAnimalsB-LymphocytesCell MovementDNA Mutational AnalysisHematopoietic Stem CellsHematopoietic SystemImmunity, InnateInterferon-gammaInterleukin-17Interleukin-2Lymphocyte ActivationActinsAdaptor Proteins, Signal TransducingHem1 protein, mouseInterferon-gammaInterleukin-17Interleukin-2Membrane Proteins

Identifiers

PMID19015308
PMCPMC2585840
OpenAlexW2140722334

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.