HMGB1 and p38 have a common regulator TGF-beta

HMGB1 is regulated by TGF-beta
TGF-beta upregulates HMGB1 expression Positive_regulation(C: TGF-beta, T: Gene_expression(T: HMGB1)) Confidence: High Inflammatory cytokines and TGF-beta increase HMGB1 expression and secretion by monocyte/macrophages. Described in 1 sentence
TGF-beta downregulates HMGB1 Negative_regulation(C: TGF-beta, T: HMGB1) Confidence: Average IFN-gamma, TNF-alpha, TWEAK, and TGF-beta induced an intracellular redistribution of HMGB1 and stimulated secretion by THP-1 cells and human blood monocytes. Described in 1 sentence
TGF-beta upregulates HMGB1 Positive_regulation(C: TGF-beta, T: HMGB1) Confidence: Low Treatment of wild-type cells with small interfering RNA to knock down OPN reduced transforming growth factor-beta1-induced alpha-smooth muscle actin and HMGB1 to levels observed in OPN-null cells. Described in 1 sentence

p38 is regulated by TGF-beta
TGF-beta downregulates p38 expression Negative_regulation(C: TGF-beta, T: Gene_expression(T: p38)) Confidence: Very high The expression of Col I and alpha-SMA in SRV4 could be reduced by SA-B independent TGF-beta1. Described in 1 sentence
TGF-beta upregulates p38 transcription Positive_regulation(C: TGF-beta, T: Transcription(T: p38)) Confidence: Very high Transforming growth factor-beta (TGF-beta) stimulates the transcription of the alpha2(I) collagen gene. Described in 2 sentences
TGF-beta upregulates p38 phosphorylation Positive_regulation(C: TGF-beta, T: Phosphorylation(T: p38)) Confidence: High As shown in Figure 4a, Western blotting revealed that TGF-beta1 induced the phosphorylation of p38-MAPK and PKC as early as 10 minutes after stimulation. Described in 41 sentences
TGF-beta upregulates p38 Positive_regulation(C: TGF-beta, T: p38) Confidence: High As tubular epithelial cells are the natural targets of TGF-beta1 in vivo [17], this result further supported that TGF-beta1 exerts its fibrogenic effect through Sema4C-mediated activation of p38 MAPK. Described in 114 sentences
TGF-beta upregulates p38 expression Positive_regulation(C: TGF-beta, T: Gene_expression(T: p38)) Confidence: Average Fluvastatin abolished TGF-beta1-induced phosphorylation of p38 MAPK and TGF-beta1-induced TSP-1 expression. Described in 11 sentences
TGF-beta regulates p38 expression Regulation(C: TGF-beta, T: Gene_expression(T: p38)) Confidence: Average The effects of TGF-beta1 on expression levels of PKCalpha and p38 MAPK. Described in 1 sentence
TGF-beta downregulates p38 Negative_regulation(C: TGF-beta, T: p38) Confidence: Low Our findings however add new insights into the TGFbeta1-mediated regulation of p38MAPK since a concentration dependence of TGFbeta on p38MAPK was revealed: Whereas low concentrations of TGFbeta1, endogenous and (0.01 ng/ml), induced p38MAPK activation, 0.1 ng/ml and 1.0 ng/ml TGFbeta prevented activation of p38MAPK. Described in 4 sentences
TGF-beta regulates p38 Regulation(C: TGF-beta, T: p38) Confidence: Low Although this claim is beyond the scope of this paper, it may be worth investigating other upstream mediators that control p38 MAPK, ERK, and AKT simultaneously such as TGF-beta, H-ras, and ASK-1, which are known to be involved in wound healing. Described in 6 sentences
Upregulation of p38 expression by TGF-beta is upregulated by TGF-beta Positive_regulation(C: TGF-beta, T: Positive_regulation(C: TGF-beta, T: Gene_expression(T: p38))) Confidence: Low Fluvastatin abolished TGF-beta1-induced phosphorylation of p38 MAPK and TGF-beta1-induced TSP-1 expression. Described in 1 sentence
Upregulation of TGF-beta upregulates p38 phosphorylation Positive_regulation(C: Positive_regulation(T: TGF-beta), T: Phosphorylation(T: p38)) Confidence: Low As shown in Figure 8A and 8B, TGFbeta2 stimulation caused phosphorylation of p38 MAPK, which was transiently upregulated at 6 h as previously reported [13]. Described in 2 sentences
TGF-beta binding upregulates p38 expression Positive_regulation(C: Binding(T: TGF-beta), T: Gene_expression(T: p38)) Confidence: Low We also show that the ligation of alpha2beta1 leads to the activation of p38 MAPK, especially its p38alpha isoform. Described in 2 sentences
Upregulation of TGF-beta upregulates p38 Positive_regulation(C: Positive_regulation(T: TGF-beta), T: p38) Confidence: Very low In non-Smad signaling pathways, activated TGF-beta receptors utilize extracellular signal-regulated kinases (ERK), P38 mitogen-activated protein kinases (p38MAPK), or c-Jun N-terminal kinases (JNK) signaling proteins to activate gene targets [41]. Described in 2 sentences
TGF-beta expression downregulates p38 expression Negative_regulation(C: Gene_expression(T: TGF-beta), T: Gene_expression(T: p38)) Confidence: Very low Transfection of the same keratinocytes with the kinase-negative mutants of p38-alpha or p38-beta mitogen-activated protein kinase markedly inhibited keratinocyte migration on collagen. Described in 1 sentence

All interactions mentioned for the specific gene symbol in text. The results are not restricted to any specific organism.

All interactions for genes that have these gene symbols as official name or synonym. The results are restricted to specific organisms and synonyms are taken into account.

All interactions for families that contain genes with these gene symbols as official name or synonym. The results group interologs and regulogs together, and synonyms are taken into account for each gene in the gene family.

All interactions mentioned between these specific gene symbols in text. The results are not restricted to any specific organism.

All interactions between genes that have these gene symbols as official name or synonym. The results are restricted to specific organisms and synonyms are taken into account.

All interactions between families that contain genes with these gene symbols as official name or synonym. The results group interologs and regulogs together, and synonyms are taken into account for each gene in the gene family.

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