Evidence map›Paper›PMID 31475084›Full record

Article3 Biotech2019

Data-independent acquisition of the proteomics of spleens from chickens infected by avian leukosis virus.

Fei Ye, Qijian He, Yan Wang, Can Cui, Fuling Yang, Bin Luo, Huadong Yin, Xiaoling Zhao, Diyan Li, Hengyong Xu and 2 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in 3 Biotech, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. 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

12 authors at 1 institution in 1 country.

Fei Ye *1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Qijian He *1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Yan Wang *1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Can Cui1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Fuling Yang1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Bin Luo1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Huadong Yin1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Xiaoling Zhao1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Diyan Li1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Hengyong Xu1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Hua Li1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Qing Zhu1Institute of Animal Genetics and Breeding, Sichuan Agricultural University, Chengdu, 611130 Sichuan China.
Sichuan Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunosuppression caused by avian leukemia virus J subgroup (ALV-J) infection includes atrophy or regeneration disorders of the lymphoid organs, decreased immune response, and termination of B lymphocyte maturation process and inhibition of T-lymphocyte development. The regulatory mechanism of the related resistance genes and protein expression is not clear. While searching for a molecular marker for the immune response to ALV-J infection, we detected differentially expressed proteins (DEPs) of spleens from chicken infected by ALV-J at 15th day and 30th day by the data-independent acquisition technique. Approximately 220 DEPs from the spleens of chickens infected by ALV-J were detected. To find a relatively stable biomarker molecule, we summarized the DEPs at two timepoints and selected activating signal cointegrator 1 complex subunit 3 (ASCC3), TBC1 domain family member 2 (TBC1D2), MHC class II beta chain 1 (BLB2), ensconsin (MAP7), complement component 1 Q subcomponent B chain (C1QB), and Follistatin-like 1 (FSTL1) from both comparisons for protein interaction network analysis. ASCC3, BLB2, C1QB, and FSTL1 were potential biomarkers for the complex infection mechanism of ALV-J and the dynamic immune mechanism of the body.

Indexed as

ALV-JASCC3BLB2C1QBFSTL1Proteomic

Identifiers

PMID31475084
PMCPMC6702595
OpenAlexW2967386588

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.