Table 5 DEGs with an important regulatory function in biological processes induced by algae extracts
#DEG | full name | function | dominant biological process | identified pathway | regulation by ETEC (h) | regulation by algae extracts in the presence of ETEC |
|---|---|---|---|---|---|---|
ANXA1 | Annexin A1 | anti-inflammatory activity / cell polarisation and cell migration | cell motility | Smooth Muscle Contraction | up (2 h) | up-regulated by S alone and slight enhancement of ETEC-induced up-regulation by S-ETEC mixture |
BTRC | Beta-Transducin Repeat Containing E3 Ubiquitin Protein Ligase | ubiquitinates phosphorylated NFKBIA, targeting it for degradation and activating nuclear factor kappa-B. | Transforming Growth Factor (TGF) | TGF-beta Receptor Signalling Pathway | down (2 h) | slight enhancement of ETEC-induced down-regulation by C-ETEC and H-ETEC mixtures |
ISG15 | ISG15 Ubiquitin-Like Modifier | regulation of antiviral response | translation (protein synthesis) and antigen recognition | Influenza Viral RNA Transcription and Replication | up (2 h) | up-regulated by S and S-ETEC mixture and silencing of ETEC-induced up-regulation by C-ETEC and H-ETEC mixtures |
MYLK | Myosin Light Chain Kinase | gastrointestinal motility, vascular permeability, leukocyte diapedesis | cell motility | Smooth Muscle Contraction | none (2 h) | down-regulation by C and H was abrogated by C-ETEC and H-ETEC mixtures |
PIAS2 | Protein Inhibitor Of Activated STAT 2 | inhibition of transcription by STAT2 in immune processes | Transforming Growth Factor (TGF) | TGF-beta Receptor Signalling Pathway | none (2 h) | down-regulated by H-ETEC mixture |
NFKBIA | NFKB Inhibitor Alpha | inhibition of transcription by NFKB in immune processes | antigen recognition / inflammation | Toll-Like Receptor Signalling Pathways | none (2 h) | up-regulated by mixtures of C-ETEC and H-ETEC |
CASP10 | Caspase 10 | execution-phase of cell apoptosis | tumour necrosis factor (inflammation) and apoptosis | TNFR1 Pathway | none (6 h) | up-regulated by mixtures of C-ETEC, H-ETEC and S-ETEC, and by AM in the presence and absence of ETEC |
HMOX1 | Heme Oxygenase 1 | Cyto-protection effects / blood vessel widening | angiogenesis (blood vessel growth) and oxidative stress | Keap1-Nrf2 Pathway / angiogenesis (CST) | none (6 h) | variable up-regulation by C, H, S, AM in the presence and absence of ETEC |
HSPA1A/B | Heat Shock Protein Family A (Hsp70) Member 1A | control of protein folding and degradation | heat shock (stress) and tumour necrosis factor (inflammation) | TNFR1 Pathway | none (6 h) | up-regulated by mixtures of AM-ETEC, C-ETEC and S-ETEC, and by AM in the absence of ETEC |
NFKBIE | NFKB Inhibitor Epsilon | inhibition of transcription by NFKB in immune processes | tumour necrosis factor (inflammation) | TNFR1 Pathway | up (6 h) | silencing of ETEC-induced up-regulation by AM-ETEC, C-ETEC, and H-ETEC mixtures |
TNFAIP3 | TNF Alpha Induced Protein 3 | termination of NF-kappa-B activity and production of inflammatory cytokines | tumour necrosis factor (inflammation) and apoptosis | TNFR1 Pathway | up (6 h) | silencing of ETEC-induced up-regulation by AM-ETEC and C-ETEC mixtures |
SPARC | Secreted Protein Acidic And Cysteine Rich | extracellular matrix synthesis and regulation of cell shape | extra cellular matrix structure | Cell Adhesion / ECM Remodelling | none (6 h) | down-regulation by AM alone and by AM-ETEC and C-ETEC mixture |