Evidence map›Paper›PMID 31751474›Full record

ArticleBlood advances2019

Sptlc1 is essential for myeloid differentiation and hematopoietic homeostasis.

Velayoudame Parthibane, Diwash Acharya, Sargur Madabushi Srideshikan, Jing Lin, Dru G Myerscough, Thiruvaimozhi Abimannan, Nagampalli Vijaykrishna, Daniel Blankenberg, Lavanya Bondada, Kimberly D Klarmann and 6 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

12 citing papers in PubMed, 10 citations in OpenAlex.

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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

16 authors at 3 institutions in 1 country.

Velayoudame ParthibaneCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Diwash AcharyaCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Sargur Madabushi SrideshikanCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Jing LinCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Dru G MyerscoughCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Thiruvaimozhi AbimannanCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Nagampalli VijaykrishnaGenomic Medicine Institute and.
Daniel BlankenbergGenomic Medicine Institute and.
Lavanya BondadaCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Kimberly D KlarmannMouse Cancer Genetics Program and.
Stephen D FoxMass Spectrometry Group, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD; and.
Thorkell AndressonMass Spectrometry Group, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD; and.
Lino TessarolloMouse Cancer Genetics Program and.
Usha AcharyaCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
Jonathan R KellerMouse Cancer Genetics Program and.
Jairaj K AcharyaCancer and Developmental Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD.
National Institutes of Health · USCancer Genetics (United States) · USCleveland Clinic Lerner College of Medicine · US

Funding

Adaptation to ceramide involves AKT/FOXO regulated novel triglyceride lipasesR01GM110288 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ACHARYA, USHA R · 2015 to 2018
$1.4M
NIGMS NIH HHS R01 GM110288
6 · The paper itself

Abstract

Serine palmitoyltransferase (SPT) long-chain base subunit 1 (SPTLC1) is 1 of the 2 main catalytic subunits of the SPT complex, which catalyzes the first and rate-limiting step of sphingolipid biosynthesis. Here, we show that Sptlc1 deletion in adult bone marrow (BM) cells results in defective myeloid differentiation. In chimeric mice from noncompetitive BM transplant assays, there was an expansion of the Lin- c-Kit+ Sca-1+ compartment due to increased multipotent progenitor production, but myeloid differentiation was severely compromised. We also show that defective biogenesis of sphingolipids in the endoplasmic reticulum (ER) leads to ER stress that affects myeloid differentiation. Furthermore, we demonstrate that transient accumulation of fatty acid, a substrate for sphingolipid biosynthesis, could be partially responsible for the ER stress. Independently, we find that ER stress in general, such as that induced by the chemical thapsigargin or the fatty acid palmitic acid, compromises myeloid differentiation in culture. These results identify perturbed sphingolipid metabolism as a source of ER stress, which may produce diverse pathological effects related to differential cell-type sensitivity.

Indexed as

HomeostasisAnimalsBone Marrow CellsCell DifferentiationComputational BiologyGene DeletionGene Expression ProfilingHematopoiesisHematopoietic Stem CellsHumansMiceMice, KnockoutMyeloid CellsMyeloid Progenitor CellsSerine C-PalmitoyltransferaseSpleenSerine C-PalmitoyltransferaseSPTLC1 protein, human

Identifiers

PMID31751474
PMCPMC6880889
OpenAlexW2990928417

What OpenQuestion holds

Textmetadata
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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.