Evidence map›Paper›PMID 15831469›Full record

ArticleMolecular and cellular biology2005

Targeted disruption of Tgif, the mouse ortholog of a human holoprosencephaly gene, does not result in holoprosencephaly in mice.

Jun Shen, Christopher A Walsh

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. Article
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  7. Review
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  10. Review
  11. Down-regulation of ATF1 leads to early neuroectoderm differentiation of human embryonic stem cells by increasing the expression level of SOX2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  12. Article
  13. Article
  14. Functions of TGIF homeodomain proteins and their roles in normal brain development and holoprosencephaly.American journal of medical genetics. Part C, Seminars in medical genetics · 2018
    Article
  15. Article
  16. Tgif1 and Tgif2 Repress Expression of the RabGAP Evi5l.Molecular and cellular biology · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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 at 2 institutions in 1 country.

Jun ShenDepartment of Neurology, Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, NRB 266, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Christopher A Walsh
Beth Israel Deaconess Medical Center · USHoward Hughes Medical Institute · US

Funding

Cell Identity Determination In Human Brain: Somatic Mutation and Cell LineageR01NS032457 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI Alice Eunjung Lee, Christopher A. Walsh · 1995 to 2026
$12.7M
SHARED RESOURCE FOR TRANSGENIC MOUSE MODELS OF CANCERR24CA083034 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TENEN, DANIEL G · 1999 to 2003
$870k
NCI NIH HHS R24 CA 83034NINDS NIH HHS R01 NS 032457NINDS NIH HHS R01 NS032457
6 · The paper itself

Abstract

5'-TG-3'-interacting factor or transforming growth factor beta (TGF-beta)-induced factor (TGIF) belongs to a family of evolutionarily conserved proteins that are characterized by an atypical three-amino-acid loop extension homeodomain. In vitro studies have implicated TGIF as a transcriptional repressor and corepressor in retinoid and TGF-beta signaling pathways that regulate several important biological processes. Heterozygous nonsense and missense mutations of the human TGIF gene have been associated with holoprosencephaly, the most common congenital malformation of the forebrain. In mice, Tgif mRNA is expressed ubiquitously in the ventricular neuroepithelium at embryonic day 10.5 (E10.5) but displays a medial to lateral gradient in the developing cerebral cortex at E12.5. The expression quickly declines by E14.5. The spatiotemporal expression profile of Tgif is consistent with its involvement in midline forebrain development. To better understand the function of Tgif in forebrain patterning and proliferation in vivo, we generated mice lacking Tgif by targeted deletion of exons 2 and 3, which encode 98% of the amino acids. Tgif(-)(/)(-) mice had no detectable Tgif protein by Western blotting. Surprisingly, however, these mice were viable and fertile. In addition, there were no discernible derangements in any of the major organ systems, including the forebrain. Overall our results point to a possible functional redundancy of Tgif, potentially provided by the closely related Tgif2.

Indexed as

AnimalsEmbryo, MammalianEmbryonic DevelopmentExonsGene ExpressionGene SilencingGene TargetingHedgehog ProteinsHoloprosencephalyHomeodomain ProteinsHumansMiceMice, KnockoutProsencephalonRepressor ProteinsRNA, MessengerHedgehog ProteinsHomeodomain ProteinsRepressor ProteinsRNA, MessengerShh protein, mouseTeratogensTGIF1 protein, humanTgif1 protein, mouseTrans-ActivatorsTretinoin

Identifiers

PMID15831469
PMCPMC1084278
OpenAlexW2152958709

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.