| 2008 |
STRIP1 (FAM40A) is a novel component of the STRIPAK complex, a large multiprotein assembly containing PP2A catalytic and scaffolding subunits, striatins (PP2A B''' regulatory subunits), Mob3, STRIP2, CCM3, and germinal center kinase III family Ste20 kinases; STRIPAK establishes mutually exclusive interactions with either CTTNBP2 proteins or a subcomplex of SLMAP/SIKE/FGFR1OP2. |
Iterative affinity purification/mass spectrometry (AP-MS) interaction mapping |
Molecular & cellular proteomics : MCP |
High |
18782753
|
| 2011 |
FAM40A (STRIP1) depletion by RNAi reduces cell spreading and alters actin filament distribution in human cells, while FAM40B (STRIP2) depletion causes cell elongation and tail retraction defects, indicating that the two paralogs have distinct functions in cytoskeletal organization and cell migration. |
RNAi knockdown with morphological phenotype scoring (cell shape, actin staining, migration assay) |
BMC biology |
Medium |
21834987
|
| 2012 |
In yeast, Far11 (ortholog of FAM40A/STRIP1) interacts physically with PP2A components Tpd3 and Pph21, and genetic epistasis shows that deletion of Far11 or PP2A subunits suppresses lethality caused by TORC2 deficiency (lst8Δ, tor2-21), placing Far11 as an antagonist of TORC2 signaling via PP2A. |
Genetic suppressor screen, co-immunoprecipitation, phosphorylation assay of TORC2 substrate Slm1 |
Genetics |
High |
22298706
|
| 2014 |
FAM40A (STRIP1) negatively regulates MST3 and MST4 kinases within the STRIPAK complex; loss of FAM40A promotes co-localization of contractile actomyosin machinery with ERM proteins via MST3/4-mediated phosphorylation of PPP1CB inhibitors (PPP1R14A-D), reducing cell speed on planar surfaces but favouring migration in confined environments. FAM40B mutations found in human tumours uncouple it from PP2A, enabling a contractile phenotype. |
RNAi knockdown, computational modelling, in vitro migration assays, in vivo breast cancer metastasis assays, co-immunoprecipitation |
Nature cell biology |
High |
25531779
|
| 2016 |
FARL-11, the C. elegans ortholog of STRIP1/2, localizes to the endoplasmic reticulum and is required for cell cycle-dependent ER morphological changes in embryos; in the germline, FARL-11 is required for normal ER morphology and for proper membrane localization of the GLP-1/Notch receptor, which is necessary for germline stem cell maintenance. |
Loss-of-function genetic analysis, immunofluorescence localization, GLP-1 receptor membrane localization assay in C. elegans |
Development (Cambridge, England) |
Medium |
27510976
|
| 2017 |
STRIP1 is essential for mesoderm migration in vivo in mouse embryos; Strip1-null mutants arrest at midgestation with failure of anterior axial mesoderm extension, and cultured mesoderm cells from null mutants show decreased spreading, abnormal focal adhesions, disorganized actin cytoskeleton, and reduced migration velocity. |
Mouse knockout, embryo phenotyping, mesoderm explant culture, mouse embryonic fibroblast migration assays, immunofluorescence for focal adhesions and actin |
Proceedings of the National Academy of Sciences of the United States of America |
High |
29203676
|
| 2018 |
FAM40A (STRIP1) interacts with CCM3 and its knockdown in endothelial cells increases stress fibers and reduces in vitro angiogenic loop formation; these effects are reverted by ROCK kinase inhibition, placing STRIP1 upstream of ROCK-mediated endothelial contractility. |
RNAi knockdown, co-immunoprecipitation, stress fiber quantification, in vitro angiogenesis assay, ROCK inhibitor rescue |
BMC cell biology |
Medium |
30509168
|
| 2018 |
FAM40A (STRIP1) localizes to the nucleus and perinuclear zone in mouse podocytes; its silencing or over-expression alters podocyte morphology and F-actin organization, and a point mutant (p521M>T) causes blunted podocyte morphology, disordered F-actin distribution, and reduced nephrin expression, demonstrating a role in podocyte cytoskeletal integrity. |
siRNA knockdown, overexpression, mutant overexpression, immunofluorescence, RT-qPCR, Western blot in mouse podocytes |
Archives of medical science : AMS |
Medium |
30697267
|
| 2019 |
Within the STRIPAK-Hippo complex, STRIP1 constitutes one of two 'arms' by which STRN3 controls loading of the Hippo kinase MST2; a decreased cell density triggers dissociation of the STRIP1 arm from STRIPAK, reflecting dynamic assembly of the complex in response to upstream signals. Disrupting the STRIP1-containing arm abrogates STRIPAK's regulatory effect on Hippo signaling. |
Co-immunoprecipitation, crystallography (defining STRN3-SIKE1 and SIKE1-SLMAP interfaces), cell-density-dependent dissociation assay, functional Hippo pathway reporter assay |
Cell discovery |
High |
30622739
|
| 2021 |
Cryo-EM structure of the human STRIPAK core (PP2AA, PP2AC, STRN3, STRIP1, MOB4) at 3.2-Å resolution reveals that STRIPAK is a non-canonical PP2A complex: it contains four copies of STRN3 forming an elongated homotetrameric coiled-coil scaffold. STRIP1 incorporates an inositol hexakisphosphate (IP6) as a structural cofactor. Mutations at subunit interfaces disrupt complex integrity and cause aberrant Hippo pathway activation. |
Cryo-EM structure determination, interface mutagenesis, Hippo pathway activation assay |
Nature structural & molecular biology |
High |
33633399
|
| 2020 |
Loss of STRIP1 in MDA-MB-231 breast cancer cells induces cell cycle arrest and decreased proliferation through induction of CDK inhibitors p21 and p27; this induction occurs in a subpopulation with low DNA damage response (p21high/γH2AXlow), and is rescued by co-depletion of MST3 and MST4 kinases, placing STRIP1 upstream of MST3/4 in regulation of p21/p27. |
RNAi knockdown, flow cytometry, single-cell immunofluorescence for p21/γH2AX, MST3/4 co-depletion rescue |
Frontiers in cell and developmental biology |
Medium |
32258031
|
| 2022 |
In zebrafish, Strip1 interacts with Striatin 3 (Strn3) and both are required for retinal ganglion cell (RGC) survival; loss of Strip1 or Strn3 activates the pro-apoptotic transcription factor Jun in RGCs, and Jun knockdown rescues RGC survival in strip1 mutants, placing Strip1 upstream of Jun-mediated apoptosis. Strip1 is additionally required for RGC dendritic patterning. |
Zebrafish genetic mutant analysis, co-immunoprecipitation (Strip1-Strn3 interaction), Jun activation assay, morpholino-mediated Jun knockdown rescue |
eLife |
High |
35314028
|
| 2023 |
In C. elegans, FARL-11 (STRIP1/2 ortholog) and CASH-1 (striatin) form a complex in vivo and both localize to the sarcoplasmic reticulum (SR); missense mutations or single-amino-acid deletions in farl-11 or cash-1 cause sarcomere disorganization, disruption of SR organization around M-lines, and altered levels of the SR Ca²⁺ release channel UNC-68. |
Co-immunoprecipitation, immunofluorescence localization, genetic missense/deletion mutant analysis, immunoblot for UNC-68 levels in C. elegans |
Molecular biology of the cell |
High |
37314837
|
| 2024 |
Strip1 localizes to the nucleolus in neonatal rat ventricular cardiomyocytes (NRVCMs) and acts as a negative regulator of cardiomyocyte hypertrophy; Strip1 knockdown increases cell size and activates the hypertrophic gene program, whereas its expression is reduced in human dilated and ischemic cardiomyopathies. Mechanistically, Strip1 associates with cardiac STRIPAK and modulates MST1/MST2 and MST4 kinase activities, influencing Hippo- and Calcineurin/NFAT-related pro-hypertrophic signaling. Morpholino-driven Strip1 reduction in zebrafish causes impaired cardiac function. |
siRNA knockdown in NRVCMs, immunofluorescence for nucleolar localization, co-immunoprecipitation for STRIPAK association, kinase activity assay (MST1/2/4), zebrafish morpholino knockdown cardiac function assay |
Cells |
Medium |
41892331
|