Evidence map›Paper›PMID 38343377›Full record

ArticleAnimal biotechnology2024

PI3K/AKT/mTORC1 signalling pathway regulates

Yongjin Mao, Chen Su, Huilin Yang, Xiaocong Ma, Feng Zhao, Bo Qu, Yang Yang, Xiaoming Hou, Bing Zhao, Yingjun Cui

Open access · diamondAbstract read
In one paragraph

Article in Animal biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Journal of inflammation research · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Exploring the therapeutic potential andFrontiers in pharmacology · 2025
    Article
  10. Article
  11. 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

10 authors at 1 institution in 1 country.

Yongjin MaoKey Laboratory of Dairy Science of Education Ministry, Northeast Agricultural University, Harbin, PR China.
Chen SuKey Laboratory of Dairy Science of Education Ministry, Northeast Agricultural University, Harbin, PR China.
Huilin YangKey Laboratory of Dairy Science of Education Ministry, Northeast Agricultural University, Harbin, PR China.
Xiaocong MaKey Laboratory of Dairy Science of Education Ministry, Northeast Agricultural University, Harbin, PR China.
Feng ZhaoKey Laboratory of Dairy Science of Education Ministry, Northeast Agricultural University, Harbin, PR China.ORCID 0000-0002-7919-6880
Bo QuKey Laboratory of Dairy Science of Education Ministry, Northeast Agricultural University, Harbin, PR China.
Yang YangKey Laboratory of Animal Cellular and Genetics Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin, PR China.
Xiaoming HouKey Laboratory of Animal Cellular and Genetics Engineering of Heilongjiang Province, Northeast Agricultural University, Harbin, PR China.
Bing ZhaoCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, PR China.
Yingjun CuiKey Laboratory of Dairy Science of Education Ministry, Northeast Agricultural University, Harbin, PR China.
Northeast Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Matrix metalloproteinase 9 (MMP9) plays a pivotal role in mammary ductal morphogenesis, angiogenesis and glandular tissue architecture remodeling. However, the molecular mechanism of MMP9 expression in mammary epithelial cells of dairy cows remains unclear. This study aimed to explore the underlying mechanism of MMP9 expression. In this study, to determine whether the PI3K/AKT/mTORC1/NF-κB signalling pathway participates in the regulation of MMP9 expression, we treated mammary epithelial cells with specific pharmacological inhibitors of PI3K (LY294002), mTORC1 (Rapamycin) or NF-κB (Celastrol), respectively. Western blotting results indicated that LY294002, Rapamycin and Celastrol markedly decreased MMP9 expression and P65 nuclear translocation. Furthermore, we found that NF-κB (P65) overexpression resulted in elevated expression of MMP9 protein and activation of MMP9 promoter. In addition, we observed that Celastrol markedly decreases P65-overexpression-induced MMP9 promoter activity. Moreover, the results of the promoter assay indicated that the core regulation sequence for MMP9 promoter activation may be located at -420 ∼ -80 bp downstream from the transcription start site. These observations indicated that the PI3K/AKT/mTORC1 signalling pathway is involved in MMP9 expression by regulating MMP9 promoter activity

Indexed as

NF-kappa BPentacyclic TriterpenesProto-Oncogene Proteins c-aktAnimalsCattleEpithelial CellsFemaleMatrix Metalloproteinase 9Mechanistic Target of Rapamycin Complex 1Phosphatidylinositol 3-KinasesSirolimusTranscriptional ActivationcelastrolMatrix Metalloproteinase 9Mechanistic Target of Rapamycin Complex 1NF-kappa BPentacyclic TriterpenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSirolimusDairy cowmammary epithelial cellsmatrix metalloproteinase 9 (MMP9)NF-κB

Identifiers

PMID38343377
PMCPMC12674440
OpenAlexW4391752296

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.