Table 3.

Finite/primary cell lines

Cell line	Tissue Origin and Morphology	References	CNF1 Described Effects	CNF1 Preparation
HPECC (HPCEC)	hu colon, finite cell line, epithelial	[22]	cell motility decrease	recombinant, purified by chromatography
HDMEC (Human Dermal Microvascular Endothelial Cells)	hu dermal, finite cell line, microvascular endothelial cells	[70,79]	Rac1, Cdc42, and RhoA activation Cdc42 protein increase stress fiber formation marked peripheral actin Rac1 and cortactin translocation to cell junctions enhanced claudin 5 immunostaining intensity tight junction linearization slight decrease of monolayer permeability	recombinant, GST fusion protein
HUVEC (Human Umbilical Vein Endothelial Cell)	hu umbilical, finite cell line, endothelial	[8,10,11,28,80]	Rho, Rac, and Cdc42 transient activation Rho, Rac, and Cdc42 efficient depletion stress fiber formation F-actin accumulation at junctional borders enhanced migration and invasion protection from barrier-disruptive agents (thrombin) p38 MAPK and c-Jun phosphorylation IκB-α depletion Rac- and Cdc42-dependent induction of inflammatory mediators-encoding genes (microarray) E-selectin, MCP-1, MIP-3α, IL-8, IL-6, TRAF1 proteins increase	recombinant, purified by chromatography, His-tagged protein
IEC-6 (Intestinal Epithelioid Cell line #6)	rat small intestine, finite cell line, epithelial	[22,81]	transient Rho, Rac, and Cdc42 activation ATP production increase increase in the activity of complex V (ATP synthase) Rho- and Rac-dependent enrichment of mitochondrial network (mitochondria elongation) Bcl-2 protein expression decrease Drp1 phosphorylation (Ser637) cAMP content increase PKA activity increase vimentin expression decrease in the presence of supernatant from activated immune cells: − cell motility increase − transient Snail1 protein upregulation	recombinant, purified by chromatography
T-lymphocytes	hu blood, primary, lymphocyte	[44]	Rho activation F-actin content increase formation of pseudopodia and filopodia-like projections clustering of CD29, CD11a and CD49d integrins into filopodia enhanced SDF1α-induced migration across acellular filters enhanced adherence to epithelial cells disruption of the epithelial cell monolayer transient p42-44MAPK and JNK activation TNF-α and TGF-β mRNA increase TNF-α and TGF-β secretion increase	recombinant, purified by chromatography
NK	hu blood, primary, large granular lymphocyte	[82]	transient Rac activation increased F-actin polarization in contact region between NK and NK-target cell increased cytotoxicity increased binding to the target cell recruitment of a higher number of effector cells on the same target cell increased CD69, CD18, ICAM-1, IL-2R, and HLA-DR proteins	recombinant, purified by chromatography
monocytes	hu blood, primary, monocyte	[60]	Rho activation lamellipodia and knob-like protuberance formation cell spreading disorganization of actin microfilaments (concentration of F-actin in foci) actin cable formation decreased ingestion of unopsonized zymosan (CR3 mediated) modulation of CR3 activation of and its colocalization with actin cytoskeleton clustering of CD11b, CD32 and CD18 in peripheral patches decreased colocalization of CD11b, CD18, and CR3 with F-actin	recombinant, purified by chromatography
macrophages	hu blood, primary, macrophage	[11]	Rho, Rac, and Cdc42 depletion	recombinant, purified by chromatography
DC (dendritic cell) monocytes	hu blood, primary, monocyte	[83]	phenotypic and functional maturation of moDCs: − increased CD83 and CD86 double-positive cell number − increased surface expression of HLA-DR MHC class II molecules − increased secretion of IL-6 and TNF-α − increased capacity to induce proliferation of allogenic naïve CD4+ T-lymphocytes	recombinant, purified by chromatography
HBMEC (Human Brain Microvascular Endothelial Cells)	hu brain, primary, microvascular endothelium	[3]	RhoA activation increased E. coli E44 invasion	recombinant, GST fusion protein
keratinocytes	hu neonatal foreskin, primary, keratinocyte	[11]	RhoA, Rac1, and Cdc42 depletion	recombinant, purified by chromatography
MERRF (Myoclonic Epilepsy with Ragged-Red Fibers) fibroblasts	hu skin, primary, from myoclonic epilepsy with ragged-red fibers, fibroblast	[84]	increase in stress fiber number and thickness, rescuing wild-type phenotype rescue of the mitochondrial morphology ATP content increase Tom20 expression increase	recombinant, purified by chromatography
fibroblasts	hu skin/neonatal foreskin, primary, fibroblast	[11,84]	RhoA, Rac1, and Cdc42 depletion stress fiber increase ATP content increase Tom20 expression increase	recombinant, purified by chromatography
BMDM (Bone-Marrow-Derived Macrophages)	mouse bone marrow derived macrophages	[85] * [61] §	reduced phagocytosis of nonopsonized beads and of E. coli CD36 mRNA and protein downregulation (partially through Cdc42-LXRβ signaling axis and C/EBPα) NLRP3 inflammasome activation (through Rac2 and PAK1) caspase-1 activation IL-1β protein maturation and secretion	recombinant, * purified by chromatography § His-tagged protein
MEFs (Mouse Embryonic Fibroblasts)	mouse embryo, primary, fibroblast	[11]	transient RhoA activation RhoA, Rac1, and Cdc42 depletion	recombinant, purified by chromatography
mouse peritoneal macrophages	mouse peritoneal lavage, primary, macrophage	[61]	reduced phagocytosis of nonopsonized E. coli CD36 mRNA and protein downregulation (partially through Cdc42-LXRβ signaling axis and C/EBPα)	recombinant, His-tagged protein
rat mesangial primary cells	rat kidney, primary	[86]	increase of Cox2 mRNA levels	recombinant, His-tagged protein
rat embryonic primary astrocytes	rat embryo cortex, primary, astrocytes	[87]	reduction of GFAP protein levels reduction of IL-1β levels reduction of glutamate-dependent intracellular Ca2+ rise transformation of astrocytes in an efficient substrate for neuritogenesis and synaptogenesis (in vitro)	recombinant, purified by chromatography
rat embryonic primary neurons	rat embryonic hippocampus	[87]	partially reversible block of neuronal differentiation (less evident in in the presence of astrocytes): − development of filopodia-like protrusions along neurites and around cell bodies − thick and tortuous dendrite formation − lack of synapse formation and reduced synaptic density − poor dendritic branching − colocalization of pre- (synaptophysin) and post-synaptic markers (PSD95) on differentiated neurons: − synapse remodeling − decreased synaptophysin positive dots	recombinant, purified by chromatography
rat embryonic primary neurons	rat newborn hippocampus	[88]	dendrite and axon retraction	recombinant, GST-fusion
rat embryonic primary neurons	rat embryonic substantia nigra	[89]	increase in neuronal process length and complexity activation of structural plasticity	recombinant, His-SUMO tag protein
OPC (Oligodendrocyte Precursor Cells)	rat/mouse newborn cortex, primary	[90]	RhoA and Rac1 activation increase of myelin sheet formation	recombinant, GST fusion protein
PAEC (Porcine Aorta Endothelial Cells)	pig pulmonary artery, primary, endothelial	[70]	RhoA. Rac1, and Cdc42 activation stress fiber formation increased peripheral F-actin staining VE-cadherin fragmentation intercellular gap formation Rho-dependent increase in cell monolayer permeability	recombinant, GST fusion protein
dog thyroid epithelial cells	dog thyroid, primary, epithelial-like	[91]	Rac1 and Cdc42 activation Rac1 depletion rescue from forskolin-induced stress fiber disruption counteraction of forskolin-dependent induction of thyroid differentiation genes (Tg, NIS, and ThOXs)	recombinant, GST fusion protein

* purified by chromatography; § His-tagged protein