Cold shock proteins: from cellular mechanisms to pathophysiology and disease

Lindquist, Jonathan A.; Mertens, Peter R.

doi:10.1186/s12964-018-0274-6

Cell Communication and Signaling

Table 2 Genes regulated by cold shock proteins in disease

From: Cold shock proteins: from cellular mechanisms to pathophysiology and disease

Protein	Disease	Target Cell	Mode of Action	Target Gene	Ref.
YB-1	Sepsis	neutrophils, macrophages	N.D.	Toll-like receptor 4 (TLR4) CXCL-1	[123]
	T-cell activation Autoimmunity Inflammation	T-helper cells	binding and stabilization of mRNA	Interleukin 2 (IL-2)	[129, 204]
	Allergic asthma	activated eosinophils	stabilization and up-regulation of mRNA transcripts	GM-CSF	[140]
		embryonic lung fibroblasts	suppression of gene transcription	GM-CSF	[205]
	Chronic liver disease	activated hepatic stellate cells	induction of expression; antagonizes TGFβ signaling	Smad7	[153]
	Chronic liver disease	rat hepatoma cells (FAO)	suppression of gene transcription	Mrp2	[206]
	Kidney transplant rejection	primary monocytes	activation of gene transcription	RANTES/CCL5	[126]
	Kidney transplant rejection	differentiated macrophages	suppression of gene transcription	RANTES/CCL5	[126]
	Neointimal hyperplasia Atherosclerosis	vascular smooth muscle cells	activation of gene transcription	RANTES/CCL5	[127]
	Endometriosis	peritoneal macrophages	activation of gene transcription and recruitment of inflammatory cells	RANTES/CCL5*	[207, 208]
	Chronic kidney disease Interstial kidney disease	proximal tubular cells	control of translation	TGFβ	[132, 209]
	Mesangioproliferative glomerulonephritis	endothelial cells	gene transcription	PDGF-B	[111]
	Mesangioproliferative glomerulonephritis	renal cells	gene transcription, secretion	PDGF-B	[138]
	Tubulointerstial nephritis	renal cells, macrophages	gene transcription, secretion, differentiation, phagocytosis	RANTES/CCL5 MCP-1/CCL2 IL-10	[124, 203]
	Dysregulated angiogenesis		repression of VEGF promotor	VEGF	[210]
	Calcineurin inhibitor mediated kidney fibrosis	mesangial cells	binding and stabilization of mRNA	Collagen	[136]
	Anti-Thy1.1 nephritis	mesangial cells	gene transcription, secretion	Notch-3	[54]
	Type II diabetes	skeletal muscle	gene transcription, signal pathways	PTP1B	[55]
	T-ALL	T cell	Cell cycle	Cdk6	[181]
CHSP1	Inflammation Sepsis	macrophages	enhancement of mRNA stability	TNF	[24]
DbpA	Dysregulated angiogenesis	fibroblasts	repression of VEGF promoter	VEGF	[130, 210]
	Hepatocellular carcinoma	hepatocytes			[211,212,213,214]
	Mesangioproliferative glomerulonephritis	renal cells	gene transcription, secretion	DbpA	[13]

For the studied cold shock domain proteins, the disease, target cell, mode of action, and target genes are listed, together with the relevant citation. In sepsis, the mode of action has not been determined (N.D.). Modified from Lindquist et al. [4].

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ISSN: 1478-811X

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