Article in Stem cell reviews and reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 49% 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
2 citing papers in PubMed, 6 citations in OpenAlex.
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 2 countries.
Yingchao NieProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01605, USA.
Qi LiProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01605, USA.
Alla AmcheslavskyProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01605, USA.
Juan Carlos DuhartSchool of Life Sciences, University of Nevada Las Vegas, Las Vegas, NV, 89154, USA.
Alexey VeraksaDepartment of Biology, University of Massachusetts Boston, Boston, MA, 02125, USA.
Hugo StockerInstitute of Molecular Systems Biology, ETH Zürich, Zürich, Switzerland.
Laurel A RafterySchool of Life Sciences, University of Nevada Las Vegas, Las Vegas, NV, 89154, USA.
Y Tony IpProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01605, USA. Tony.Ip@umassmed.edu.
University of Massachusetts Chan Medical School · USUniversity of Nevada, Las Vegas · USETH Zurich · CHUniversity of Massachusetts Boston · US
Funding
Outreach/Diversity/Pipeline ProjectP20GM103440 · NIGMS · UNIVERSITY OF NEVADA RENO · PI Eduardo A Robleto · 2012 to 2026
$58.0M
PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
University of Massachusetts Center for Clinical and Translational ScienceUL1TR000161 · NCATS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LUZURIAGA, KATHERINE F · 2012 to 2015
$11.0M
Genetic analysis of damage-induced intestinal stem cell division in DrosophilaR01DK083450 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI IP, Y. TONY · 2010 to 2024
$4.7M
TGF-BETA FAMILY REGULATION OF EPITHELIAL MORPHOGENESISR01GM060501 · NIGMS · UNIVERSITY OF NEVADA LAS VEGAS · PI RAFTERY, LAUREL A · 2000 to 2012
$4.5M
Homeostatic signaling in the Drosophila intestineR01GM107457 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI IP, Y. TONY · 2015 to 2018
$1.3M
Steroid-Dependent Changes in the Yorkie InteractomeR01GM105813 · NIGMS · EMORY UNIVERSITY · PI MOBERG, KENNETH H, VERAKSA, ALEXEY · 2013 to 2016
The Drosophila adult midgut contains intestinal stem cells that support homeostasis and repair. We show here that the leucine zipper protein Bunched and the adaptor protein Madm are novel regulators of intestinal stem cells. MARCM mutant clonal analysis and cell type specific RNAi revealed that Bunched and Madm were required within intestinal stem cells for proliferation. Transgenic expression of a tagged Bunched showed a cytoplasmic localization in midgut precursors, and the addition of a nuclear localization signal to Bunched reduced its function to cooperate with Madm to increase intestinal stem cell proliferation. Furthermore, the elevated cell growth and 4EBP phosphorylation phenotypes induced by loss of Tuberous Sclerosis Complex or overexpression of Rheb were suppressed by the loss of Bunched or Madm. Therefore, while the mammalian homolog of Bunched, TSC-22, is able to regulate transcription and suppress cancer cell proliferation, our data suggest the model that Bunched and Madm functionally interact with the TOR pathway in the cytoplasm to regulate the growth and subsequent division of intestinal stem cells.
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.
Bunched and Madm Function Downstream of Tuberous Sclerosis Complex to Regulate the Growth of Intestinal Stem Cells in Drosophila. · full record | OpenQuestion