| 2013 |
PKD1 phosphorylates and inhibits SSH1L (SSH1) downstream of RhoA/PLCε signaling in cardiomyocytes. SSH1L inhibition prevents cofilin 2 translocation to mitochondria and blocks Bax mitochondrial translocation, thereby promoting cell survival after oxidative stress/ischemia-reperfusion injury. |
Genetic knockdown (SSH1L siRNA), pharmacological manipulation, western blotting for cofilin phosphorylation, mitochondrial fractionation, cardiomyocyte survival assays; epistasis established RhoA→PLCε→PKD1→SSH1L→cofilin2 pathway |
Science signaling |
High |
24345679
|
| 2014 |
SSH1 directly interacts with NOD1 at F-actin-rich sites and is an essential component of the NOD1 innate immune signaling pathway; SSH1-mediated cofilin activation is required for NOD1-dependent NF-κB activation and cytokine release. Cytochalasin D (actin polymerization inhibitor) rescued NOD1 signaling loss upon SSH1 depletion. |
Genome-wide siRNA screen, co-immunoprecipitation/interaction assay showing NOD1-SSH1 interaction at F-actin sites, NF-κB reporter assay, cytokine measurement, chemical rescue with cytochalasin D |
PLoS pathogens |
High |
25187968
|
| 2015 |
SSH1 (SSH1L) acts as a cofilin-1 phosphatase in pancreatic cancer cells; SSH1L knockdown increased cofilin-1 Ser3 phosphorylation (inactivation) and inhibited cell migration without affecting proliferation. Cytochalasin D abrogated migration independently of SSH1L expression. |
siRNA-mediated knockdown of SSH1L in PC cell lines, western blotting for phospho-cofilin-1 (Ser3), wound-healing/migration assays, cytochalasin D rescue |
Cancer letters |
Medium |
25684665
|
| 2004 |
Missense mutation p.Ser63Asn and frameshift mutations in SSH1 were identified in families with disseminated superficial actinic porokeratosis (DSAP), implicating SSH1 phosphatase function in epidermal cytoskeleton organization. |
Genome-wide linkage analysis, candidate gene sequencing, mutation identification in affected families |
Human mutation |
Medium |
15459975
|
| 2019 |
In zebrafish cardiomyocytes, the mechanosensitive protein vinculin (VCL) recruits SSH1 and its effector cofilin (CFL) to regulate F-actin rearrangement and promote myofilament maturation in response to mechanical forces from heartbeat contraction. |
VCL interactome by mass spectrometry in contracting vs. non-contracting cardiomyocytes, co-immunoprecipitation, loss-of-function studies, live imaging of F-actin; genetic epistasis (VCL→SSH1→CFL) |
Developmental cell |
High |
31495694
|
| 2018 |
PKCδ activates SSH1 in macrophages, which dephosphorylates cofilin at Ser3, leading to membrane ruffle formation and macropinocytosis. SSH1 silencing blocked cofilin dephosphorylation and inhibited macropinocytosis stimulated by phorbol ester or HGF. |
siRNA knockdown of SSH1, western blot for phospho-cofilin, scanning electron microscopy of ruffles, flow cytometry (FITC-dextran internalization), pharmacological inhibitors |
Cellular signalling |
Medium |
30261270
|
| 2020 |
SSH1 dephosphorylates phospho-Ser403-SQSTM1/p62, thereby impairing SQSTM1 autophagic flux and reducing clearance of phospho-MAPT/tau. This action is fully dependent on SQSTM1 Ser403 phosphorylation status and is mechanistically separable from SSH1-mediated cofilin dephosphorylation. |
RNAi knockdown and overexpression of SSH1, genetically encoded fluorescent reporters, defined phospho-site mutant constructs, western blotting, proximity ligation assay, experiments in cell lines, primary neurons, and mouse brains |
Autophagy |
High |
33044112
|
| 2020 |
NRP2 activates SSH1 in endothelial cells, which in turn activates cofilin to promote F-actin polymerization, HUVEC migration, and PNET angiogenesis via a VEGF/VEGFR2-independent pathway. SSH1 silencing blocked NRP2-induced cofilin activation and cell migration. |
siRNA knockdown of SSH1, western blot for cofilin phosphorylation, F-actin staining, wound-healing/tube formation assays, in vivo mouse PNET model |
Cell & bioscience |
Medium |
32983407
|
| 2023 |
SSH1 promotes intrahepatic cholangiocarcinoma (iCCA) cell proliferation, migration, and invasion through activation of the p38 MAPK pathway and enhanced expression of CXCL8. |
SSH1 overexpression and knockdown in iCCA cell lines, western blotting for p38 MAPK pathway components, CXCL8 measurement, proliferation/migration/invasion assays |
Carcinogenesis |
Medium |
36857607
|
| 2023 |
CRISPR-mediated SSH1 knockout or pharmacological inhibition suppressed HCC cell viability, migration, and invasion, and downregulated WNT/β-catenin pathway components (WNT3, β-catenin, LRP5/6) and circadian clock regulators (CLOCK, BMAL1), while upregulating CFL-1/2 and CRY1. |
CRISPR SSH1 knockout, pharmacological inhibition (Sennoside A), cell viability/migration/invasion assays, western blotting, in vivo mouse tumor model |
Aging |
Medium |
37837551
|
| 2024 |
SSH1 modulates neuropathic pain and neuronal health in the medial prefrontal cortex by dephosphorylating cofilin and LIMK1; co-immunoprecipitation demonstrated interaction between SSH1 and LIMK1. |
Lentiviral overexpression and knockdown of SSH1 in mouse mPFC, behavioral assays, western blotting for p-cofilin and p-LIMK1, co-immunoprecipitation, immunofluorescence |
Experimental cell research |
Medium |
39701356
|
| 2025 |
RBMS1 promotes glioma cell proliferation through a c-Myc-SSH1 axis: RBMS1 induces c-Myc binding to SSH1 promoters, increasing SSH1 expression, which in turn supports proliferative behavior. |
Patient datasets, glioma cell lines, mouse xenograft models, chromatin immunoprecipitation (c-Myc binding to SSH1 promoter), knockdown/overexpression experiments, proliferation assays |
Biochemical and biophysical research communications |
Medium |
40120347
|