Evidence map›Paper›PMID 29735529›Full record

ArticleThe Journal of biological chemistry2018

Global loss of leucine carboxyl methyltransferase-1 causes severe defects in fetal liver hematopoiesis.

Jocelyn A Lee, Zhengqi Wang, Danielle Sambo, Kevin D Bunting, David C Pallas

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. HES1 is required for mouse fetal hematopoiesis.Stem cell research & therapy · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. 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

5 authors at 4 institutions in 2 countries.

Jocelyn A LeeFrom the Department of Biochemistry, Winship Cancer Institute, the Biochemistry, Cell, and Developmental Graduate Program, and.
Zhengqi Wangthe Aflac Cancer and Blood Disorders Center of Children's Healthcare of Atlanta, Department of Pediatrics, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia 30322.
Danielle SamboFrom the Department of Biochemistry, Winship Cancer Institute, the Biochemistry, Cell, and Developmental Graduate Program, and.
Kevin D Buntingthe Aflac Cancer and Blood Disorders Center of Children's Healthcare of Atlanta, Department of Pediatrics, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia 30322.
David C PallasFrom the Department of Biochemistry, Winship Cancer Institute, the Biochemistry, Cell, and Developmental Graduate Program, and dpallas@emory.edu.
Winship Cancer InstituteCancer Institute (WIA) · INChildren's Healthcare of Atlanta · USEmory University · US

Funding

Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
STAT5 Structure-Function in HematopoiesisR01DK059380 · NIDDK · EMORY UNIVERSITY · PI BUNTING, KEVIN D · 2002 to 2017
$4.2M
ROLE OF PP2A IN POLYOMAVIRUS TUMOR ANTIGEN FUNCTIONSR01CA057327 · NCI · EMORY UNIVERSITY · PI PALLAS, DAVID C · 1992 to 2012
$4.1M
Specificity and function of PP2A carboxymethylationF31CA123640 · NCI · EMORY UNIVERSITY · PI LEE, JOCELYN ANNE · 2006 to 2009
$132k
NCI NIH HHS F31 CA123640NCI NIH HHS P30 CA138292NCI NIH HHS R01 CA057327NIDDK NIH HHS R01 DK059380
6 · The paper itself

Abstract

Leucine carboxyl methyltransferase-1 (LCMT-1) methylates the C-terminal leucine α-carboxyl group of the catalytic subunits of the protein phosphatase 2A (PP2A) subfamily of protein phosphatases, PP2Ac, PP4c, and PP6c. LCMT-1 differentially regulates the formation and function of a subset of the heterotrimeric complexes that PP2A and PP4 form with their regulatory subunits. Global LCMT-1 knockout causes embryonic lethality in mice, but LCMT-1 function in development is unknown. In this study, we analyzed the effects of global LCMT-1 loss on embryonic development. LCMT-1 knockout causes loss of PP2Ac methylation, indicating that LCMT-1 is the sole PP2Ac methyltransferase. PP2A heterotrimers containing the Bα and Bδ B-type subunits are dramatically reduced in whole embryos, and the steady-state levels of PP2Ac and the PP2A structural A subunit are also down ∼30%. Strikingly, global loss of LCMT-1 causes severe defects in fetal hematopoiesis and usually death by embryonic day 16.5. Fetal livers of homozygous

Indexed as

HematopoiesisAnimalsApoptosisCell ProliferationDNA MethylationEmbryo, MammalianFetusLiverMiceMice, KnockoutProtein O-MethyltransferaseProtein Phosphatase 2Lcmt1 protein, mouseProtein O-MethyltransferaseProtein Phosphatase 2developmenthematopoiesisLCMT-1mouseprotein phosphatase 2 (PP2A)protein phosphatase methyltransferaseprotein serine/threonine phosphatase (PSP)

Identifiers

PMID29735529
PMCPMC6016458
OpenAlexW2799780361

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.