Evidence map›Paper›PMID 30600463›Full record

ArticleCytotechnology2019

NSP-C contributes to the upregulation of CLOCK/BMAL1-mediated transcription.

Hiroshi Hosoda, Satoshi Kida

Open access · bronzeAbstract read
In one paragraph

Article in Cytotechnology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 55% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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 1 institution in 1 country.

Hiroshi HosodaDepartment of Molecular Microbiology, Faculty of Life Science, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo, 156-8502, Japan.
Satoshi KidaDepartment of Bioscience, Faculty of Life Science, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo, 156-8502, Japan. kida@nodai.ac.jp.ORCID http://orcid.org/0000-0002-8038-9583
Tokyo University of Agriculture · JP

Funding

Challenging Exploratory Research KAKENHI 17K19464Challenging Exploratory Research KAKENHI 24650172Challenging Exploratory Research KAKENHI 26640014Scientific Research (A) KAKENHI 15H02488Scientific Research (A) KAKENHI 18H03944Scientific Research (B) KAKENHI 20380078Scientific Research (B) KAKENHI 23300120Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 17H05581Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 17H05961Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 17H06084Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 18H05428Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 18H05434Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 23115716Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 24116001Scientific Research on Innovative Areas (Research in a proposed research area) KAKENHI 24116008Scientific Research on Priority Areas - Molecular Brain Science- KAKENHI 18022038Scientific Research on Priority Areas - Molecular Brain Science- KAKENHI 22022039
6 · The paper itself

Abstract

The bHLH-PAS transcription factors clock circadian regulator (CLOCK) and brain and muscle ARNT-like protein 1 (BMAL1) play essential roles in the generation of circadian gene expression rhythms through the activation of E-box-mediated transcription. Importantly, circadian transcriptional rhythms mediated by CLOCK/BMAL1 are observed in peripheral tissues as well as in the suprachiasmatic nucleus and contribute to tissue-specific functions. These findings suggest that CLOCK/BMAL1 have roles in many biological phenomena by interacting with various cellular regulators. In the present study, to understand the mechanisms underlying the multiple functional roles of CLOCK, we tried to identify new proteins that interact with CLOCK using a yeast two-hybrid system. We identified neuroendocrine-specific protein (NSP)-C, which is highly expressed in the brain, as a positive regulator of CLOCK/BMAL1-mediated transcription. We found that NSP-C interacted with CLOCK in mammalian cells. Co-expression of NSP-C with CLOCK/BMAL1 enhanced the transcriptional activation by CLOCK/BMAL1. Furthermore, knockdown of endogenous NSP-C by small interfering RNA (siRNA) suppressed E-box-mediated transcription, while this reduction of transcription was rescued by the expression of NSP-C protected from the action of siRNA. These observations suggest that NSP-C contributes to the upregulation of CLOCK/BMAL1-mediated transcription.

Indexed as

CLOCKInteractionNSP-CTranscription activationYeast-two hybrid

Identifiers

PMID30600463
PMCPMC6368517
OpenAlexW2907655209

What Socratic 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 Socratic graph.