Evidence map›Paper›PMID 26728456›Full record

ArticleThe Journal of biological chemistry2016

SREBP2 Activation Induces Hepatic Long-chain Acyl-CoA Synthetase 1 (ACSL1) Expression in Vivo and in Vitro through a Sterol Regulatory Element (SRE) Motif of the ACSL1 C-promoter.

Amar Bahadur Singh, Chin Fung Kelvin Kan, Bin Dong, Jingwen Liu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

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  17. ACSL1 affects Triglyceride Levels through the PPARγ Pathway.International journal of medical sciences · 2020
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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

4 authors at 1 institution in 1 country.

Amar Bahadur SinghFrom the Department of Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304.
Chin Fung Kelvin KanFrom the Department of Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304.
Bin DongFrom the Department of Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304.
Jingwen LiuFrom the Department of Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304 Jingwen.Liu@va.gov.
VA Palo Alto Health Care System · US

Funding

Targeting PCSK9 Transcription to Combat Hypercholesterolemia by BerberineR01AT006336 · NCCIH · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI LIU, JINGWEN · 2012 to 2016
$1.7M
NCCIH NIH HHS 1R01AT006336-01A1NCCIH NIH HHS R01 AT006336
6 · The paper itself

Abstract

Long-chain acyl-CoA synthetase 1 (ACSL1) plays a key role in fatty acid metabolism. To identify novel transcriptional modulators of ACSL1, we examined ACSL1 expression in liver tissues of hamsters fed a normal diet, a high fat diet, or a high cholesterol and high fat diet (HCHFD). Feeding hamsters HCHFD markedly reduced hepatic Acsl1 mRNA and protein levels as well as acyl-CoA synthetase activity. Decreases in Acsl1 expression strongly correlated with reductions in hepatic Srebp2 mRNA level and mature Srebp2 protein abundance. Conversely, administration of rosuvastatin (RSV) to hamsters increased hepatic Acsl1 expression. These new findings were reproduced in mice treated with RSV or fed the HCHFD. Furthermore, the RSV induction of acyl-CoA activity in mouse liver resulted in increases in plasma and hepatic cholesterol ester concentrations and reductions in free cholesterol amounts. Investigations on different ACSL1 transcript variants in HepG2 cells revealed that the mRNA expression of C-ACSL1 was specifically regulated by the sterol regulatory element (SRE)-binding protein (SREBP) pathway, and RSV treatment increased the C-ACSL1 abundance from a minor mRNA species to an abundant transcript. We analyzed 5'-flanking sequence of exon 1C of the human ACSL1 gene and identified one putative SRE site. By performing a promoter activity assay and DNA binding assays, we firmly demonstrated the key role of this SRE motif in SREBP2-mediated activation of C-ACSL1 gene transcription. Finally, we demonstrated that knockdown of endogenous SREBP2 in HepG2 cells lowered ACSL1 mRNA and protein levels. Altogether, this work discovered an unprecedented link between ACSL1 and SREBP2 via the specific regulation of the C-ACSL1 transcript.

Indexed as

Response ElementsAnimalsBinding SitesCholesterolCoenzyme A LigasesCricetinaeDiet, High-FatHep G2 CellsHumansLiverMaleMesocricetusMiceMice, Inbred C57BLProtein BindingRNA, MessengerACSL1 protein, humanCholesterolCoenzyme A LigasesRNA, MessengerSterol Regulatory Element Binding Protein 2ACSL1acyl-CoA synthetasedietary cholesterolfatty acid metabolismlipid metabolismliverSREBPstatintranscription promotertranscription regulation

Identifiers

PMID26728456
PMCPMC4777867
OpenAlexW2289081239

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.