Serum response factor: Look into the gut

Table 1 Identified roles of SRF in the GI tract

GI system	Process involved	Molecules associated	GI disorder associated
Esophagus	Myofibroblast differentiation[19]	TGFβ, ILK	Ulcer
Stomach	Angiogenesis[20]	VEGF, Rho-actin, MEK-ERK	Ulcer
Stomach	Re-epithelialization, muscular structure restoration[6]	Actin, immediate-early genes	Ulcer
Stomach	H. pylori activates SRF[21,22]	CagA, villin	Intestinal metaplasia
Intestine	Smooth muscle contraction[23,24]	Smooth muscle actin, smooth muscle myosin, smoothelin, F/G actin	Intestinal obstruction, CIPO
Colon	Alternative splicing, cell survival[26]	SRFΔ5, K-ras	Colon cancer
Liver	Cell cycle; hepatocyte proliferation/survival[29,30]	IGF-1	Liver injury
Liver	Cell proliferation, cell cycle, apoptosis[33]	E2F1	Hepatocellular carcinoma
Liver	Cell invasion[31]	E-cadherin, β-catenin	Liver metastasis
Pancreas	Cell proliferation[32]	Pro-inflammatory cytokines	Pancreatitis

SRF: Serum response factor; GI: Gastrointestinal; TGF: Transforming growth factor; VEGF: Vascular endothelial growth factor; MEK: Mitogen-activated protein kinase kinase; ERK: Extracellular regulated kinase; H. pylori: Helicobacter pylori; IGF: Insulin-like growth factors; CIPO: Chronic intestinal pseudo-obstruction.

Table 2 Tools and models available to study SRF functions in GI

Tool	Purpose	Model
SRF in pcDNA3.1, His[6,21]	SRF over-expression	Gene therapy
SRF antisense sequence[21,33]	SRF down-regulation (siRNA)	Gene depletion
Srf Flex1 mice[35]	Conditional in vivo SRF deletion	Gene depletion
Srf loxP mice[30]	Conditional in vivo SRF deletion	Gene depletion
CreER T2 mice[36]	SMS tissue expression	CIPO
AlfpCre mice[31]	Hepatocyte tissue expression	Liver function
K5-Cre mice[37]	Squamous epithelial expression	Esophagus, foregut
Fabp/Cre mice[38]	Conditional gut tissue expression	Small/large intestine
H. pylori[23]	H. pylori infection in human cell lines (in vitro) or mice (in vivo)	H. pylori gastric diseases