ArticleApoptosis : an international journal on programmed cell death2015
Apoptosis transcriptional mechanism of feline infectious peritonitis virus infected cells.
Article in Apoptosis : an international journal on programmed cell death, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Circulation and Genetic Characterizations of Coronaviruses From Companion Animals in Chengdu, Southwest China: One-Year Postpandemic.Transboundary and emerging diseases · 2025Article
- Whole blood RNA profiling in cats dissects the host immunological response during recovery from feline infectious peritonitis.PloS one · 2025Article
- Cross-Linking Mass Spectrometry to Capture Protein Network Dynamics of Cell Membranome.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Baicalin Inhibits FIPV Infection In Vitro by Modulating the PI3K-AKT Pathway and Apoptosis Pathway.International journal of molecular sciences · 2024Article
- Transcriptomics-based anti-tuberculous mechanism of traditional Chinese polyherbal preparation NiuBeiXiaoHe intermediates.Frontiers in pharmacology · 2024Article
- Natural selection differences detected in key protein domains between non-pathogenic and pathogenic Feline Coronavirus phenotypes.bioRxiv : the preprint server for biology · 2023Article
- Natural selection differences detected in key protein domains between non-pathogenic and pathogenic feline coronavirus phenotypes.Virus evolution · 2023Article
- Epidemiology and Comparative Analyses of the S Gene on Feline Coronavirus in Central China.Pathogens (Basel, Switzerland) · 2022Article
- Review
- Animal Coronaviruses Induced Apoptosis.Life (Basel, Switzerland) · 2021Review
- Comprehensive Transcriptomic Analysis Identifies Novel Antiviral Factors Against Influenza A Virus Infection.Frontiers in immunology · 2021Article
- The Effect of Natural Feline Coronavirus Infection on the Host Immune Response: A Whole-Transcriptome Analysis of the Mesenteric Lymph Nodes in Cats with and without Feline Infectious Peritonitis.Pathogens (Basel, Switzerland) · 2020Article
- Cellular Metabolic Profiling of CrFK Cells Infected with Feline Infectious Peritonitis Virus Using Phenotype Microarrays.Pathogens (Basel, Switzerland) · 2020Article
- Characterization of peritoneal cells from cats with experimentally-induced feline infectious peritonitis (FIP) using RNA-seq.Veterinary research · 2018Article
- Expression profiles of immune mediators in feline Coronavirus-infected cells and clinical samples of feline Coronavirus-positive cats.BMC veterinary research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis has been postulated to play an important role during feline infectious peritonitis virus (FIPV) infection; however, its mechanism is not well characterized. This study is focused on apoptosis and transcriptional profiling of FIPV-infected cells following in vitro infection of CRFK cells with FIPV 79-1146 WSU. Flow cytometry was used to determine mode of cell death in first 42 h post infection (hpi). FIPV infected cells underwent early apoptosis at 9 hpi (p < 0.05) followed by late apoptosis at 12 hpi (p < 0.05) and necrosis from 24 hpi (p < 0.05). Then, next generation sequencing was performed on 9 hpi and control uninfected cells by Illumina analyzer. An aggregate of 4546 genes (2229 down-regulated and 2317 up-regulated) from 17 cellular process, 11 molecular functions and 130 possible biological pathways were affected by FIPV. 131 genes from apoptosis cluster (80 down-regulated and 51 up-regulated) along with increase of apoptosis, p53, p38 MAPK, VEGF and chemokines/cytokines signaling pathways were probably involved in apoptosis process. Six of the de-regulated genes expression (RASSF1, BATF2, MAGEB16, PDCD5, TNFα and TRAF2) and TNFα protein concentration were analyzed by RT-qPCR and ELISA, respectively, at different time-points. Up-regulations of both pro-apoptotic (i.e. PDCD5) and anti-apoptotic (i.e. TRAF2) were detected from first hpi and continuing to deregulate during apoptosis process in the infected cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.