| 1999 |
Human Slit2 acts as a chemorepellent for olfactory and hippocampal axons and collapses their growth cones, functioning through Robo1 and Robo2 receptors in the developing forebrain. |
Collagen gel repulsion assay, growth cone collapse assay using recombinant human Slit2 |
Neuron |
High |
10197527
|
| 2001 |
Slit2 is proteolytically cleaved in vivo into a 140 kDa N-terminal fragment (Slit2-N) and a 55-60 kDa C-terminal fragment (Slit2-C). Only Slit2-N (and uncleaved Slit2-U) bind Robo receptors. Slit2-N repels olfactory bulb axons and induces growth cone collapse, while only Slit2-N (not Slit2-C) induces DRG axon branching. The full-length uncleaved form antagonizes branching by Slit2-N. |
Binding assays with Robo proteins, collagen gel repulsion/attraction assays, growth cone collapse assay using engineered truncated and mutant Slit2 constructs |
The Journal of neuroscience |
High |
11404413
|
| 2006 |
Slit2-induced growth cone collapse in Xenopus retinal neurons requires local protein synthesis and endocytosis; Slit2 activates MAP kinases and translation regulators in growth cones, and causes a protein-synthesis-dependent decrease in F-actin and increase in the actin-depolymerizing protein cofilin. Disruption of heparan sulfate blocks Slit2-induced protein synthesis and repulsion. |
Pharmacological inhibition of translation, endocytosis, MAPKs, and heparan sulfate; immunostaining for cofilin and F-actin in Xenopus retinal growth cones treated with Slit2-conditioned medium |
Neuron |
High |
16423696
|
| 2007 |
Slit2 inhibits CXCL12-induced chemotaxis and transendothelial migration of T cells and monocytes. CXCR4 physically associates with Robo1, and Slit2 treatment enhances this association. The CC3 motif of Robo1 mediates interaction with CXCR4. Slit2 blocks CXCL12-induced activation of Src and Lck kinases, Akt phosphorylation, and Rac activation, but not MAPK activation. |
Co-immunoprecipitation of CXCR4 and Robo1; chemotaxis and transendothelial migration assays; Western blot for kinase activation; domain deletion mutants of Robo1 |
Journal of leukocyte biology |
Medium |
17565045
|
| 2008 |
Slit-2 mediates tumor-suppressive effects in breast cancer cells through coordinated regulation of the β-catenin and PI3K signaling pathways and by enhancing β-catenin/E-cadherin-mediated cell-cell adhesion. |
Slit2 overexpression in MCF-7 cells; in vitro proliferation and migration assays; in vivo tumor growth in mouse models; Western blot for β-catenin and PI3K pathway components |
The Journal of biological chemistry |
Medium |
18611862
|
| 2009 |
Slit2 promotes vascular stability through Robo4 by forming a Robo4-paxillin complex at the cell surface that blocks activation of Arf6 and consequently Rac, via recruitment of Arf-GAP GIT1. This inhibits cellular protrusive activity underlying neovascularization and vascular leak. |
Co-immunoprecipitation of Robo4 with paxillin/Hic-5; biochemical assays for Arf6 and Rac activation; Arf6 inhibition in vivo (choroidal/retinal neovascularization models); cell biological protrusion assays |
Nature cell biology |
High |
19855388
|
| 2009 |
Slit2 inhibits glioma cell migration and invasion through Robo1-dependent suppression of Cdc42 activity. siRNA knockdown of Robo1 prevents Slit2-mediated Cdc42 inactivation and rescues cell migration inhibition. |
Cdc42 activity assay (GTP pull-down), Robo1 siRNA knockdown, modified Boyden chamber migration assay, in vivo intracranial tumor model |
Neuro-oncology |
Medium |
20008733
|
| 2009 |
Slit2 crystal structure of the fourth domain (D4) reveals homodimerization using conserved residues on its concave face; D4 also binds heparan sulphate. Slit2 D4 causes growth cone collapse in chick retinal ganglion cells, which can be inhibited by exogenously added heparan sulphate. |
X-ray crystallography of Slit2 D4; heparan sulphate binding assay; chick retinal ganglion cell growth cone collapse assay |
EMBO reports |
High |
19498462
|
| 2009 |
Slit2 inhibits directional migration (chemotaxis) but not random movement of neutrophils toward fMLP, C5a, and IL-8, acting through Robo1. Mechanistically, Slit2 suppresses chemoattractant-induced actin barbed-end formation, cell polarization, and activation of Cdc42 and Rac2, without impairing major kinase pathways. In vivo, Slit2 reduces neutrophil recruitment in mouse peritoneal inflammation models. |
Video-microscopic live cell tracking; actin barbed-end formation assay; Cdc42/Rac2 activation assays; mouse peritoneal inflammation models; Robo1 expression confirmed by flow cytometry |
Journal of leukocyte biology |
High |
19759280
|
| 2010 |
Slit2 differentially regulates eosinophil and neutrophil chemotaxis through differential expression of srGAP1. In eosinophils (low srGAP1), Slit2/Robo1 activates Cdc42 and recruits PI3K to Robo1, enhancing eotaxin-induced chemotaxis. In neutrophils (high srGAP1), srGAP1 binding to Robo1 leads to Cdc42 inactivation and repulsion. Aerosol Slit2 accelerates eosinophil infiltration, while IV Slit2 reduces it. |
Measurement of srGAP1 expression in eosinophils vs neutrophils; PI3K recruitment to Robo1 by co-immunoprecipitation; Cdc42 activity assays; in vivo aerosol/IV Slit2 administration in OVA-sensitized mice; siRNA blockade of srGAP1 |
Journal of immunology |
Medium |
20944010
|
| 2011 |
Slit-2 repels olfactory ensheathing cell (OEC) migration via Robo receptor. The repulsion requires Ca2+ release from internal stores through IP3 receptor channels. Slit-2-induced collapse of the leading front requires Ca2+-dependent cofilin activation (F-actin severing), while soma reversal requires spatial reversal of RhoA activity across the cell. |
Live cell imaging of OEC migration; Ca2+ imaging; pharmacological inhibition of IP3 receptors, cofilin, and RhoA/ROCK; immunostaining of cofilin activation |
Journal of cell science |
Medium |
21187345
|
| 2012 |
Slit2 is a potent inhibitor of platelet function. Robo1 is expressed on human and murine platelets and megakaryocytes. Slit2 impairs platelet adhesion and spreading by suppressing Akt activation, prevents platelet activation by ADP, prolongs bleeding times in vivo, delays vessel occlusion after arterial injury, and prevents stable occlusive thrombus formation. |
Immunofluorescence microscopy and flow cytometry for Robo1; static and shear microfluidic adhesion assays; Akt activation assays; murine tail bleeding and intravital microscopy models of arterial injury |
Circulation |
High |
22865890
|
| 2012 |
Slit2 and Robo3 directly modulate migration of GnRH neurons. Mice lacking Slit2 or Robo3 have a reduced number of GnRH neurons reaching the forebrain but normal complement of their axonal substrates, indicating a direct role on the neurons rather than via axonal patterning. |
Genetic knockout mouse models for Slit2 and Robo3; quantification of GnRH neuron numbers and axon patterns |
Development |
Medium |
22912413
|
| 2013 |
Slit2-Robo4 signaling represses LPS-induced endothelial inflammation (cytokine secretion, ICAM-1 upregulation, monocyte adhesion) by inhibiting the Pyk2-NF-κB pathway downstream of TLR4. Robo1 has proinflammatory properties and is downregulated by Slit2 via miR-218. |
siRNA knockdown of Robo1 and Robo4 in HUVECs; cytokine/ICAM-1 measurement; NF-κB and Pyk2 phosphorylation assays; monocyte adhesion assay |
Journal of immunology |
Medium |
24272999
|
| 2014 |
SLIT2 inhibits directed motility of pancreatic ductal adenocarcinoma cells through autocrine/paracrine ROBO1-mediated signaling. Restoring SLIT2 expression inhibits neural invasion and PDAC cell navigation along neurites; ROBO1 silencing in SLIT2-competent cells stimulates motility. Conditioned medium from SLIT2-competent PDAC cells impairs endothelial migration, but an N-terminal SLIT2 cleavage fragment stimulates it. |
SLIT2 restoration by transfection; ROBO1 siRNA knockdown; neural co-culture invasion assay; migration assays; in vivo tumor model |
Cancer research |
Medium |
24448236
|
| 2014 |
Fibroblasts from healthy human tissues secrete Slit2, which inhibits monocyte-to-fibrocyte differentiation. In mice, injections of Slit2 inhibit bleomycin-induced lung fibrosis. |
Slit2 identification in fibroblast conditioned medium; fibrocyte differentiation assays with recombinant Slit2; in vivo bleomycin fibrosis model with Slit2 injections |
PNAS |
Medium |
25489114
|
| 2015 |
Slit2 signals through Robo1 and Robo2 to promote retinal angiogenesis in vivo. Slit2/Robo1/Robo2 signaling promotes endothelial cell migration and is required for both Slit2- and VEGF-induced Rac1 activation and lamellipodia formation. |
Conditional knockout mice for Slit2, Robo1, Robo2 (individual and combined); postnatal retinal vascular analysis; ocular neovascular disease model; Rac1 activation and lamellipodia assays in endothelial cells |
Nature medicine |
High |
25894826
|
| 2015 |
SLIT2/ROBO1 signaling regulates mammary stem cell self-renewal by governing the choice between asymmetric and symmetric cell divisions through the transcription factor SNAI1 and the spindle orientation protein mINSC. Loss of SLIT2/ROBO1 signaling increases nuclear SNAI1, which upregulates mInsc and shifts cap cells toward symmetric divisions, expanding the stem cell pool. |
Slit2/Robo1 knockout mouse mammary gland analysis; SNAI1 overexpression; mInsc expression measurement; cell division orientation quantification; rescue by SLIT2 treatment |
Cell reports |
Medium |
26440891
|
| 2015 |
Slit2 serves as a β-catenin (Ctnnb1)-dependent retrograde signal from muscle to direct presynaptic (motoneuron) differentiation at the neuromuscular junction. Muscle-specific Ctnnb1 mutant lacking the transactivation domain fails to rescue presynaptic deficits. Transgenic Slit2 expression in muscle rescues presynaptic deficits caused by Ctnnb1 mutation. Slit2 immobilized on beads induces synaptophysin puncta in spinal cord axons. |
In vivo transgenic rescue experiments; bead-immobilized Slit2 applied to spinal cord explants; NMJ morphological analysis |
eLife |
Medium |
26159615
|
| 2015 |
Slit2/Robo1 signaling promotes intestinal tumorigenesis through Src-mediated activation of the Wnt/β-catenin pathway: Slit2/Robo1 activates Src signaling, which downregulates E-cadherin, thereby activating Wnt/β-catenin. |
Slit2 transgenic mice crossed with ApcMin/+ and DMH/DSS colorectal carcinoma models; Western blot for Src, E-cadherin, β-catenin; in vitro signaling assays |
Oncotarget |
Medium |
25605242
|
| 2015 |
CAF-secreted SLIT2 increases neurite outgrowth from dorsal root ganglia neurons and Schwann cell migration/proliferation through modulation of N-cadherin/β-catenin signaling. SLIT2/ROBO inhibition disrupts the stromal/neural connection. |
Co-culture of CAFs with DRG neurons; neurite outgrowth measurement; Schwann cell migration/proliferation assays; SLIT2/ROBO signaling inhibition; N-cadherin/β-catenin Western blot |
Cell death & disease |
Medium |
25590802
|
| 2016 |
Full-length Slit2 is cleaved to generate smaller fragments in adipose tissue and in mice. The C-terminal fragment (Slit2-C, ~50 kDa) is the active thermogenic moiety that promotes adipose thermogenesis and augments energy expenditure. Mechanistically, Slit2 induces robust PKA signaling activation, which is required for its prothermogenic activity. |
Proteomics identification of Slit2 fragments; in vivo administration of Slit2-C fragment; PKA signaling assays; pharmacological inhibition of PKA; metabolic phenotyping in mice |
Cell metabolism |
High |
26876562
|
| 2016 |
SLIT2/ROBO2 signaling inhibits nonmuscle myosin IIA (NMIIA) activity and destabilizes kidney podocyte adhesion through SRGAP1. The myosin II regulatory light chain (MRLC) directly interacts with SRGAP1, and SLIT2 treatment promotes formation of a ROBO2/SRGAP1/NMIIA complex. SLIT2 stimulation decreases focal adhesion formation and reduces podocyte attachment to collagen. Podocyte-specific Robo2 knockout protects mice from hypertension-induced podocyte detachment. |
Co-immunoprecipitation of MRLC with SRGAP1 and ROBO2; NMIIA activity assays; focal adhesion staining; collagen adhesion assays; podocyte-specific Robo2 conditional knockout mice |
JCI insight |
High |
27882344
|
| 2018 |
Slit2/Robo1 signaling promotes liver fibrosis through activation of hepatic stellate cells (HSCs). In HSCs, Robo1 neutralizing antibody and Robo1 siRNA downregulate phosphorylation of Smad2, Smad3, PI3K, and AKT independently of TGF-β1, and inhibit α-SMA expression. |
Primary mouse HSCs and LX-2 human HSC line treated with Slit2/Robo1 manipulations; Western blot for Smad2/3, PI3K, AKT; Slit2 transgenic and Robo1/2+/- mice with CCl4-induced fibrosis |
Journal of hepatology |
Medium |
26264936
|
| 2018 |
USP33 deubiquitinates and stabilizes Robo1, thereby enhancing Slit2-Robo1 inhibitory signaling in gastric cancer cells. Co-IP analysis confirmed the interaction between Robo1 and USP33; ubiquitination analysis showed USP33 reduces Robo1 ubiquitination. |
Co-immunoprecipitation of Robo1 and USP33; ubiquitination assay; migration and EMT assays after USP33 manipulation |
Cell proliferation |
Medium |
30896071
|
| 2018 |
CAPN5 directly cleaves SLIT2 in photoreceptors in vitro to generate SLIT2-N and SLIT2-C fragments. CAPN5 interacts with SLIT2 in retinal photoreceptors by co-immunoprecipitation. Increased CAPN5-mediated SLIT2 cleavage and secretion promotes PKA activation and proliferation in retinal pigment epithelium cells. |
In vitro cleavage assay (CAPN5 + SLIT2); co-immunoprecipitation in 661W cells; conditioned medium experiments; PKA activation by immunofluorescence and Western blot; CAPN5 knock-in mouse |
Investigative ophthalmology & visual science |
Medium |
29610848
|
| 2018 |
SLIT2 (expressed by CD34- orbital fibroblasts) attenuates the inflammatory phenotype of CD34+ fibrocytes in Graves' disease orbit. Conditioned medium from CD34- fibroblasts reduces MHC-2, thyroglobulin, TSHR, and AIRE expression in fibrocytes; depleting the medium of Slit2 reverses these effects. Recombinant human Slit2 mimics these effects. TSH induces Slit2 expression in GD-OF by enhancing both gene transcription and mRNA stability. |
Conditioned medium experiments with Slit2 depletion by antibody; recombinant Slit2 treatment; gene expression analysis; TSH stimulation experiments |
Journal of immunology |
Medium |
29752312
|
| 2018 |
Direct negative cross-talk exists between SLIT2 and BMP-Gremlin signaling pathways: the SLIT2-Gremlin interaction inhibits both SLIT2-ROBO2 signaling in neurons and Gremlin antagonism of BMP activity. BMP2 downregulates SLIT2 expression and promoter activity through canonical BMP/SMAD signaling; Gremlin treatment, BMP receptor inhibition, and SMAD4 knockdown rescue this repression. |
SLIT2-Gremlin binding assay; SLIT2-ROBO2 neuronal signaling assay; BMP activity assay in myoblasts; SLIT2 promoter-reporter assay; SMAD4 siRNA knockdown; BMP2 treatment of nephron progenitor cells |
The Journal of biological chemistry |
Medium |
29317497
|
| 2019 |
SLIT2 inhibits osteoclastogenesis and bone resorption through ROBO1-mediated suppression of Cdc42 activity. Binding ELISA confirmed SLIT2 directly binds ROBO1 (not ROBO3) in bone marrow-derived macrophages. Robo1 siRNA blocks SLIT2-mediated suppression of osteoclastogenesis. Cdc42 overexpression reverses SLIT2-mediated inhibition. |
Binding ELISA for SLIT2-ROBO1 interaction; Cdc42 activity assay; Robo1 siRNA knockdown; osteoclast differentiation and bone resorption assays; Cdc42 overexpression rescue |
Biochemical and biophysical research communications |
Medium |
31084928
|
| 2020 |
Tumor cell-derived double-stranded RNA activates TLR3 in endothelial cells to induce SLIT2 expression. Endothelial-derived SLIT2 and its receptor ROBO1 on tumor cells promote cancer cell migration toward endothelial cells and intravasation. Deleting endothelial Slit2 suppresses metastasis, while deleting tumoural Slit2 enhances it, demonstrating that the same gene can promote or suppress cancer depending on its cellular source. |
Genetically tagged endothelial ribosome profiling; conditional endothelial and tumor-specific Slit2 deletion in mouse breast/lung cancer models; TLR3 activation studies; in vitro migration assays; endogenous retroviral element RNA detection |
Nature |
High |
32999457
|
| 2020 |
SLIT2 inhibits macropinocytosis in macrophages and RAS-transformed cancer cells by inducing cytoskeletal changes via Roundabout receptors. In vivo, SLIT2 attenuates muramyl dipeptide uptake, preventing NOD2-dependent NF-κB activation and CXCL1 secretion. Blocking endogenous SLIT2 enhances CXCL1 secretion. |
Macropinocytosis assays in macrophages and RAS-transformed cells; in vivo SLIT2 administration; NOD2/NF-κB pathway readouts; endogenous SLIT2 blocking experiments; CXCL1 measurement |
Nature communications |
High |
32807784
|
| 2021 |
SLIT2 promotes microglia/macrophage chemotaxis and tumor-supportive polarization in glioblastoma via ROBO1- and ROBO2-mediated PI3K-γ activation. Macrophage Robo1 and Robo2 deletion and systemic SLIT2 trap delivery mimic SLIT2 knockdown effects on tumor growth and the tumor microenvironment. |
SLIT2 knockdown in mouse glioma cells; macrophage-specific Robo1/Robo2 deletion; PI3K-γ activation assays; SLIT2 trap systemic delivery; tumor growth and immune profiling |
The Journal of clinical investigation |
High |
34181595
|
| 2021 |
Slit2 reduces breast cancer metastasis by activating M1-like tumor-associated macrophages (TAMs) and enhancing their phagocytosis of tumor cells via suppression of IL-6. Slit2 also diminishes tumor fibrosis by increasing matrix metalloproteinase 13 expression in M1-TAMs. |
Slit2 overexpression in syngeneic and xenograft mammary tumor models; in vitro and in vivo phagocytosis assays; IL-6 manipulation; MMP13 expression analysis; macrophage polarization assays |
Cancer research |
Medium |
34400395
|
| 2022 |
IGF2BP3 (an m6A reader) promotes TNBC metastasis by binding to and destabilizing m6A-methylated SLIT2 mRNA, thereby impairing SLIT2/ROBO1 downstream signaling and activating PI3K/AKT and MEK/ERK pathways. |
RNA m6A modification analysis; IGF2BP3 binding to SLIT2 mRNA; mRNA stability assays; pathway activation by Western blot; in vivo xenograft metastasis model |
FASEB journal |
Medium |
36250924
|
| 2023 |
CAF-derived SLIT2 promotes gastric cancer metastasis by binding ROBO1, which interacts with serine/threonine kinase NEK9 (identified by mass spectrometry). SLIT2 enhances ROBO1-NEK9 binding. NEK9 kinase domain interacts with ROBO1 intracellular domain. NEK9 directly phosphorylates TRIM28 and cortactin (CTTN). TRIM28 acts as a transcriptional elongation factor and, together with STAT3 and NF-κB p100, drives CTTN transcription, inducing cytoskeletal reorganization. |
Mass spectrometry identification of ROBO1 interactors; Co-IP of ROBO1 and NEK9; domain deletion analysis; in vitro kinase assay for NEK9 phosphorylation of TRIM28 and CTTN; transcriptional assays; in vitro and in vivo metastasis models |
Cell death & disease |
Medium |
37443302
|
| 2023 |
SLIT2-ROBO1 axis facilitates liver metastasis of PDAC through 'coadaptation' dependent on the dependence receptor (DR) characteristics of ROBO1. A neutralizing antibody targeting ROBO1 significantly attenuates PDAC liver metastasis by preventing the coadaptation effect. |
Mouse PDAC metastasis model with CT/3D bioluminescence imaging; ROBO1 dependence receptor characterization; ROBO1-neutralizing antibody treatment |
Nature communications |
Medium |
36792623
|
| 2016 |
ISL1-based LIM complexes (ISL1-LHX3 and ISL1-LHX4) bind to the Slit2 enhancer and drive endogenous Slit2 expression in somatic motor neurons and branchiomotor neurons. Loss of Isl1 results in near-complete absence of Slit2 transcript in brainstem motor neurons and causes cranial motor neuron positioning and axon guidance defects. |
ChIP-seq analysis showing ISL1 binding to Slit2 enhancer; Isl1 conditional knockout mice; in situ hybridization and immunostaining for Slit2; luciferase reporter assay for Slit2 enhancer |
Scientific reports |
Medium |
27819291
|
| 2004 |
EphrinA5 and slit2 both induce growth cone collapse in chick retinal ganglion cells through shared pathways (PI3K and Src family kinases) but diverge in that non-classical PKC isoforms are required for ephrinA5-mediated but not slit2-mediated collapse. PI3K and Src family kinases are co-purified by affinity chromatography with the slit2 receptor Roundabout. |
Pharmacological inhibition of PI3K, Src, and PKC in chick retinal ganglion cell growth cone collapse assay; affinity chromatography of Roundabout with PI3K; colocalization of Src and Roundabout |
Journal of neurobiology |
Medium |
15007828
|
| 2020 |
NADPH oxidase 2 (Nox2) acts downstream of slit2/Robo2 in retinal ganglion cell axon guidance. Slit2-mediated growth cone collapse, axonal retraction, and repulsive turning are eliminated by Nox inhibition. Slit2 treatment increases growth cone hydrogen peroxide levels via Nox2 activation. In vivo, astray/nox2 double heterozygotes show decreased retinotectal innervation, suggesting genetic interaction. |
Pharmacological Nox inhibition; ROS biosensor imaging in growth cones; Nox2 mutant zebrafish; double heterozygote genetic interaction analysis; in vitro growth cone collapse and turning assays |
Developmental neurobiology |
Medium |
33191581
|
| 2015 |
Slit2 promotes angiogenesis in endothelial cells via the Robo1-VEGFR2-ERK1/2 pathway. Slit2 overexpression upregulates Robo1, VEGFR2, and phosphorylated ERK1/2 in HUVECs and in laser-treated transgenic mouse retina/choroid, promoting endothelial proliferation, migration, and tube formation. |
Slit2 overexpression in HUVECs; laser-induced CNV in Slit2 transgenic mice; Western blot for VEGFR2 and p-ERK1/2; proliferation, migration, tube formation assays |
Investigative ophthalmology & visual science |
Medium |
26244297
|
| 2018 |
Slit2/Robo1 signaling promotes angiogenesis in glomerular endothelial cells under diabetic conditions through the PI3K/Akt/VEGF pathway. Robo1 siRNA suppresses PI3K/Akt and VEGF activation; PI3K inhibitor blocks VEGF but not Robo1 expression, placing Robo1 upstream of PI3K/Akt. |
Slit2 siRNA in mesangial cells; conditioned medium on glomerular endothelial cells; Robo1 siRNA; PI3K inhibitor; Western blot for PI3K/Akt/VEGF/HIF-1α; proliferation, migration, tube formation assays |
Angiogenesis |
Medium |
29299781
|
| 2020 |
Slit2-Robo1 signaling promotes cardiac fibrosis through crosstalk with the TGF-β1/Smad pathway. Recombinant Slit2 activates TGF-β1/Smad signaling in cardiac fibroblasts and upregulates collagen I and periostin; Slit2 siRNA downregulates Smad2/3 and collagen I. |
Recombinant Slit2 treatment of cardiac fibroblasts; Slit2 siRNA and TGF-β1 siRNA; Western blot for Smad2/3, collagen I, PI3K/Akt; TAC mouse model; Robo1 antagonist R5 |
ESC heart failure |
Medium |
33236535
|
| 2022 |
CCN2/CTGF directly interacts with the 7th-9th EGF repeats and C-terminal cysteine knot motif of Slit2 in hepatic stellate cells and fibrotic livers. CCN2/CTGF and Slit2 synergistically activate PI3K/AKT in primary HSCs, and soluble Robo1-Fc chimera inhibits these activities. |
Co-immunoprecipitation and domain mapping of CCN2/CTGF with Slit2; PI3K/AKT activation assays; Robo1-Fc inhibition; Ccn2/Ctgf conditional knockout mice with CCl4 fibrosis |
Journal of cell communication and signaling |
Medium |
36469291
|