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Table 1 Key findings from our analysis: Genes and pathways perturbed by BM

From: Elucidating mechanistic insights into drug action for atopic dermatitis: a systems biology approach

Gene/Pathway

Role in skin pathways

Impact derived from eSkIN

TNF pathway

TNF pathway via NF-κB regulates the transcription of inflammatory cytokines, adhesion molecules, MMP9 and SELE.

TNF and its receptors are downregulated after treatment with BM, thus effecting anti-inflammatory effect.

TLRs

TLRs play important role in inflammation by activating NF-κB, which in turn, activates inflammatory cytokines.

Downregulated after treatment with BM, thus bringing about anti-inflammatory effect.

IL4 pathway

Involved in T-cell and eosinophil chemotaxis

Downregulated after treatment with BM, thus contributes towards anti-inflammatory effect.

LOR, FLG, TGM5 and CDSN

Important skin barrier proteins

Upregulated after treatment with BM; contributes towards restoration of skin barrier functions.

IVL, Keratins, LCEs, desmocollins and desmogleins

Important skin barrier proteins

Downregulated after treatment with BM representing the damage to skin barrier; CD44, AKT1, PKC-δ, HRAS and MAP2K3 involved in pathway leading to transcriptional activation of barrier proteins are also downregulated in BM samples.

S100 family proteins

Important anti-microbial peptides that help in protecting the skin from infections.

Downregulated after treatment with BM, thus leading to impaired barrier function.

VEGF

Wound healing and cell migration, vascular permeability, angiogenesis, cell invasion and coagulation

Downregulated after treatment with BM, thus affecting wound healing and other cellular processes through PLC-γ and MAPK cascade.

H2AFX, RAD51, BRCA2, MCM3, DHFR, HMOX1, GINS1 and PCNA

Genes involved in DNA repair

Downregulated after treatment with BM, thus affecting DNA repair processes.