| 1998 |
RanBPM (RanBP9) was identified as a centrosomal protein that binds GTP-Ran and is required for microtubule nucleation; overexpression produced ectopic microtubule nucleation sites co-localizing with gamma-tubulin, and anti-RanBPM antibodies inhibited microtubule aster formation. |
Yeast two-hybrid (Ran bait), sucrose-density gradient centrifugation, immunofluorescence, antibody inhibition assays |
The Journal of cell biology |
Medium |
9817760
|
| 2001 |
The originally described 55 kDa RanBPM was a truncated isoform; the full-length protein is 90 kDa with an N-terminal proline/glutamine-rich region, forms a >670 kDa complex, and localizes predominantly to nucleus and cytoplasm surrounding the centrosome—not within the centrosome itself. |
Full-length cDNA cloning, immunoblotting with antibodies against three distinct regions, gel filtration, immunofluorescence |
Gene |
High |
11470507
|
| 2002 |
RanBPM interacts with the tyrosine kinase domain of MET receptor via its SPRY domain; RanBPM activates the Ras-Erk-SRE pathway by recruiting Sos to the MET complex, functioning as an adaptor protein. |
Yeast two-hybrid, in vitro GST pull-down, co-immunoprecipitation, Ras-GTP loading assay, ERK phosphorylation assay, SRE-luciferase reporter, cell migration assay |
The Journal of biological chemistry |
High |
12147692
|
| 2002 |
RanBPM interacts with androgen receptor (AR) and glucocorticoid receptor (GR), but not estrogen receptor, and enhances their transcriptional activity in a ligand-dependent manner when overexpressed in prostate cancer cells. |
Yeast two-hybrid, GST pull-down, His-tag pull-down, transient overexpression with luciferase reporter assays |
The Journal of biological chemistry |
Medium |
12361945
|
| 2002 |
USP11, a ubiquitin-specific protease, interacts with RanBPM and deubiquitinates it; RanBPM undergoes proteasome-dependent degradation and is ubiquitinated in vivo and in vitro, and USP11 inhibits this ubiquitination in a dose-dependent manner. |
Yeast two-hybrid, co-immunoprecipitation, pulse-chase analysis with proteasome inhibitors, in vivo and in vitro ubiquitination assays, recombinant USP11 inhibition assay |
The Biochemical journal |
High |
12084015
|
| 2002 |
HIPK2 (homeodomain-interacting protein kinase 2) interacts with RanBPM in the nucleus of mammalian cells; both wild-type HIPK2 and a kinase-dead HIPK2 mutant co-localize with RanBPM in defined nuclear structures. |
Yeast two-hybrid, co-immunoprecipitation in mammalian cells, immunofluorescence co-localization |
Biochemical and biophysical research communications |
Low |
12220523
|
| 2003 |
RanBPM forms a protein complex with Twa1 and Muskelin (hMuskelin), as demonstrated by co-immunoprecipitation and gel-filtration analysis; all three proteins share the LisH-CTLH motif. |
Yeast two-hybrid, co-immunoprecipitation, gel-filtration chromatography |
Gene |
Medium |
12559565
|
| 2003 |
RanBPM interacts with the death domain of p75NTR neurotrophin receptor intracellular domain. |
Yeast two-hybrid, co-immunoprecipitation in mammalian cells, domain mapping |
Biochemical and biophysical research communications |
Low |
12963025
|
| 2003 |
CDK11(p46), a caspase-processed apoptotic kinase, directly interacts with RanBPM via its SPRY domain and phosphorylates RanBPM in vitro. |
Yeast two-hybrid, in vitro binding assay, co-immunoprecipitation in human cells, in vitro kinase assay |
Biochemical and biophysical research communications |
Medium |
14511641
|
| 2004 |
RanBPM is a peripheral plasma membrane protein that interacts with the cytoplasmic domain of integrin LFA-1 (beta2) and beta1 integrin via in vitro and in vivo assays; RanBPM is phosphorylated on serine residues and this phosphorylation is regulated by p38 kinase activity; RanBPM synergizes with LFA-1 in AP-1-dependent transcriptional activation. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation, membrane fractionation, phosphorylation assays with p38 inhibitor SB203580, luciferase reporter assay |
The Journal of biological chemistry |
High |
14722085
|
| 2004 |
RanBPM interacts with the tyrosine kinase domain of Axl and Sky/Tyro3 receptor tyrosine kinases via its SPRY-LisH domain region; a truncated RanBPM lacking this region fails to interact with Axl; endogenous Axl and RanBPM interact constitutively in multiple mammalian cell lines. |
Yeast two-hybrid, co-immunoprecipitation in cell-free and mammalian cell systems, domain deletion analysis, Gas6 stimulation experiment |
The international journal of biochemistry & cell biology |
Medium |
15964779
|
| 2004 |
Mouse RanBPM interacts with the germline-specific RNA helicase MVH (mouse vasa homolog) in testicular germ cells; both proteins associate with perinuclear RNA-protein complexes and chromatoid bodies. |
Yeast two-hybrid, co-localization by immunofluorescence in testis |
Molecular reproduction and development |
Low |
14648869
|
| 2005 |
RanBPM interacts with p73alpha (but not p53) through the extreme C-terminal region of p73alpha; RanBPM stabilizes p73alpha by inhibiting its ubiquitination, thereby prolonging its half-life and enhancing its proapoptotic activity; co-expression causes nuclear co-localization of RanBPM and p73alpha. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation, immunofluorescence, ubiquitination assay, half-life analysis |
Oncogene |
Medium |
15558019
|
| 2005 |
RanBPM interacts with the cytoplasmic domain of neural cell adhesion molecule L1 via its N-terminal SPRY domain; overexpression of N-RanBPM reduces L1-triggered ERK1/2 activation by 50% and inhibits L1-mediated neurite outgrowth and branching. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation, L1 antibody patching/subcellular redistribution, ERK activation assay, primary neuron morphology |
Journal of neurochemistry |
Medium |
16000162
|
| 2005 |
RanBPM interacts with TAF4 (a TFIID subunit); co-transfection of TAF4 and RanBPM increases primary neurite processes in neural progenitors; the effect is abolished by a TAF4 isoform lacking the RanBPM-interacting domain. |
Protein-protein interaction screen, co-immunoprecipitation from neural stem cell extracts, co-transfection/morphology assay |
Molecular and cellular neurosciences |
Low |
15911349
|
| 2006 |
RanBPM associates with the N-terminus of CD39/ecto-NTPDase1; co-expression of RanBPM substantially reduces NTPDase activity of recombinant CD39 but not of an N-terminus-deleted CD39 mutant, demonstrating functional regulation of ecto-nucleotidase activity. |
Yeast two-hybrid, co-immunoprecipitation in transfected mammalian cells, NTPDase activity assay, domain deletion mutant analysis |
The Biochemical journal |
Medium |
16478441
|
| 2006 |
RanBPM physically interacts with Plexin-A1 and mediates Semaphorin3A signaling; overexpression of RanBPM with Plexin-A1 reduces cell spreading and inhibits axonal outgrowth in vitro and in vivo; a truncated RanBPM blocks Sema3A responsiveness; RanBPM knockdown reduces Sema3A responsiveness; the RanBPM/Plexin-A1 complex is regulated by MICAL expression. |
Domain-based interaction screen, co-immunoprecipitation, overexpression and truncation/knockdown functional assays in neurons and non-neuronal cells, in vivo axon guidance assay |
The Journal of neuroscience |
High |
16672672
|
| 2006 |
RanBPM interacts with TrkA via its SPRY motif (binding at TrkA tyrosine kinase domain); overexpression of RanBPM inhibits NGF-induced NFAT-dependent luciferase expression. |
Yeast two-hybrid, co-immunoprecipitation, GST pull-down, NFAT-luciferase reporter assay |
Neuroscience letters |
Low |
16959415
|
| 2006 |
RanBPM is a coactivator of thyroid hormone receptors (TRs); it binds TRs in a ligand-independent manner via its C-terminal region interacting with the TR DNA-binding domain; overexpression enhances TR-dependent transcriptional activation, whereas the truncated RanBPM55 lacking the N-terminal polyglutaminated region inhibits it in a dominant-negative manner. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation, transient transfection luciferase reporter, domain deletion competition assays |
Journal of molecular endocrinology |
Medium |
16595702
|
| 2007 |
RanBPM is a component of a large protein complex (renamed CTLH complex) composed of Muskelin, p48EMLP, p44CTLH, ARMC8alpha, and ARMC8beta; each component was confirmed by co-immunoprecipitation and in vitro Twa1 pull-down. |
Tandem MS with anti-RanBPM antibody immunoprecipitation from HEK293 cells, co-immunoprecipitation in Cos-7 cells, in vitro pull-down with bacterially expressed Twa1 |
Gene |
High |
17467196
|
| 2008 |
Muskelin subcellular localization is co-regulated with RanBP9; knockdown of muskelin or RanBP9 both produce protrusive cell morphologies with enlarged cell perimeters; RanBP9 binding via the muskelin C-terminus is required to restore normal morphology, identifying a muskelin-RanBP9 complex as a nucleocytoplasmic mediator of cell morphology. |
Subcellular fractionation, siRNA knockdown, rescue with cDNA variants, cell morphology quantification |
The Journal of cell biology |
Medium |
18710924
|
| 2008 |
RanBPM interacts with metabotropic glutamate receptors mGlu2 and other group II and group III receptors (except mGlu6) in the retina, co-localizing with mGlu8b in the inner plexiform layer. |
Yeast two-hybrid (mGlu8 bait), co-immunoprecipitation, immunofluorescence co-localization in retina sections |
FEBS letters |
Low |
18555800
|
| 2008 |
RanBPM interacts with p42(IP4)/Centaurin-alpha-1 via its SPRY domain; D-Ins(1,3,4,5)P4 (a specific ligand for p42(IP4)) inhibits this interaction in a concentration-dependent and stereoselective manner. |
Co-immunoprecipitation with endogenous RanBPM from rat brain, in vitro binding assay, inositol phosphate competition assay, domain mapping with SPRY domain |
Journal of neurochemistry |
Medium |
18298663
|
| 2008 |
RanBPM interacts with Rta (EBV immediate-early protein) via the SPRY domain of RanBPM; this interaction promotes Rta transactivation activity, and mechanistically RanBPM interacts with SUMO-E2 (Ubc9) to enhance sumoylation of Rta by SUMO-1. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation, confocal co-localization, transient transfection reporter assay, sumoylation assay |
Journal of molecular biology |
Medium |
18455188
|
| 2008 |
RanBPM modulates T-type Ca2+ channel Cav3.1 by binding its intracellular loop between transmembrane domains I and II; RanBPM expression increases Cav3.1 currents and abolishes PKC activator-mediated inhibition of these currents. |
Yeast two-hybrid, whole-cell patch-clamp electrophysiology, domain binding assay |
Biochemical and biophysical research communications |
Medium |
18801335
|
| 2008 |
Drosophila RanBPM is required for normal germline stem cell (GSC) niche organization; loss of the long RanBPM isoform causes defects in niche cell size, niche organization, and abnormal accumulation of adherens junction component Armadillo (beta-catenin), increasing GSC attachment to niche cap cells. |
Drosophila genetics (null and isoform-specific alleles), mosaic analysis, immunofluorescence for Armadillo and Hts |
The Journal of cell biology |
Medium |
18762575
|
| 2009 |
RanBPM promotes BACE1 cleavage of APP and Abeta generation; RanBP9 N-terminal SPRY-LisH domain interacts with LRP, APP, and BACE1 simultaneously, scaffolding these proteins together; RanBP9 reduces cell surface APP, accelerates APP internalization, and increases lipid raft association of APP; knockdown of endogenous RanBP9 significantly reduces Abeta generation in CHO cells and primary neurons. |
Co-immunoprecipitation, cell surface biotinylation, endocytosis assay, lipid raft fractionation, siRNA knockdown, Abeta ELISA |
The Journal of biological chemistry |
High |
19251705
|
| 2009 |
A processed form of RanBP9 (RanBP9-N60, residues 1-392) lacks a nuclear localization signal, displays enhanced cytoplasmic localization and >3-fold enhanced stability compared to full-length RanBP9, retains capacity to form self-interacting multimeric complexes via LisH domain, and potentiates Abeta generation ~5-fold. |
Deletion mutant analysis, subcellular fractionation, protein stability assays, Abeta ELISA |
FASEB journal |
Medium |
19729516
|
| 2009 |
RanBPM has proapoptotic activity: transient expression induces caspase activation; the C-terminal domain stimulates this activity while the central SPRY domain negatively regulates it; RanBPM knockdown prevents DNA damage-induced caspase-3 and caspase-2 activation; following ionizing radiation, RanBPM relocalizes from nucleus to cytoplasm; RanBP9 downregulation decreases mitochondria-associated Bax and increases Bcl-2. |
Transient expression, siRNA knockdown, caspase activation assay, immunofluorescence for relocalization, Bax/Bcl-2 western blot |
Molecular cancer research |
Medium |
19996306
|
| 2009 |
RanBPM interacts with acetylcholinesterase (AChE) C-terminal domain and translocates from the cytoplasm to the nucleus during cisplatin-induced apoptosis, similar to AChE. |
Yeast two-hybrid, co-immunoprecipitation, immunoblotting of cytoplasmic and nuclear fractions |
Acta biochimica et biophysica Sinica |
Low |
19902122
|
| 2010 |
RanBPM interacts with citron kinase (CITK) at adherens junctions of the neocortical ventricular surface; RanBPM knockdown decreases CITK polarization to the ventricular surface, increases mitotic cells, and decreases cytokinetic cells; the CITK mutation rescues the RanBPM knockdown mitosis phenotype, placing RanBPM upstream of CITK in M-phase progression. |
Yeast two-hybrid, co-immunoprecipitation, protein overlay, in utero RNAi, genetic epistasis with CITK mutant |
Developmental neurobiology |
Medium |
19790105
|
| 2010 |
RanBPM interacts with TrkB receptor and contributes to BDNF-induced MAPK and Akt activation; RanBPM overexpression enhances BDNF-induced MAPK/Akt signaling; RanBPM siRNA knockdown has opposite effects; RanBPM promotes BDNF-induced hippocampal neuronal morphogenesis and BDNF-mediated survival. |
Co-immunoprecipitation, overexpression and siRNA knockdown, phospho-MAPK/Akt western blot, neuronal morphology and survival assays |
Journal of neurochemistry |
Medium |
20403074
|
| 2010 |
RanBPM interacts with YPEL5 protein; RanBPM was identified as a YPEL5-binding protein and their interaction was confirmed by yeast two-hybrid. |
Yeast two-hybrid |
Genomics |
Low |
20580816
|
| 2010 |
RanBPM interacts with Mgl-1 (mammalian Lgl1); RanBPM inhibits Mgl-1 proteasomal degradation and extends its half-life; RanBPM enhances Mgl-1 activity in cell migration and colony formation assays. |
Yeast two-hybrid, co-immunoprecipitation, GST pull-down, protein stability assay, cell migration and colony formation assays |
The Journal of biological chemistry |
Medium |
20829363
|
| 2011 |
RanBPM is essential for mammalian gametogenesis: RanBPM-null mice of both sexes are sterile; males show spermatogenesis arrest at late pachytene-diplotene prophase I without chromosome synapsis defects; females show premature ovarian failure at prophase I; chimera experiments demonstrate cell-autonomous function in germ cells. |
Gene knockout in mice, histological analysis, meiotic staging, chimeric mouse generation with knockout ES cells |
Development |
High |
21561988
|
| 2012 |
RanBP9 overexpression disrupts integrin-dependent cell attachment, spreading, and focal adhesion signaling (Pyk2/paxillin), while knockdown promotes these processes; RanBP9 accelerates endocytosis of β1-integrin, LRP, and APP; primary hippocampal neurons from RanBP9-transgenic mice show reduced surface β1-integrin, LRP, APP, and neurite arborization. |
Cell attachment/spreading assays, focal adhesion immunostaining, cell surface biotinylation, endocytosis assay, siRNA knockdown, primary neuron from transgenic mice |
FASEB journal |
High |
22223749
|
| 2012 |
RanBP9 activates/dephosphorylates cofilin and promotes Abeta-induced apoptosis; siRNA knockdown of cofilin abolishes both Abeta- and RanBP9-induced apoptosis, placing cofilin downstream of RanBP9 in the apoptotic pathway. |
siRNA knockdown (cofilin, RanBP9), cofilin phosphorylation western blot, apoptosis assays (RanBP9-Tg mice), spatial memory testing |
Cell death and differentiation |
Medium |
22361682
|
| 2012 |
RanBP9 overexpression in mice leads to >2-fold increase in Abeta40 and Abeta42 levels and increased amyloid plaque deposition; RanBP9-null mice show increased synaptic protein levels (synaptophysin, PSD-95, drebrin A). |
Transgenic and null mouse generation, ELISA for Abeta, amyloid plaque immunostaining, synaptic protein western blot |
FASEB journal |
High |
22294787
|
| 2012 |
RanBPM inhibits ERK signaling by forming a complex with c-Raf, decreasing Hsp90 binding to c-Raf, and destabilizing c-Raf protein; RanBPM knockdown stimulates MEK and ERK phosphorylation leading to Bcl-2 upregulation; RanBPM expression prevents MEK/ERK activation by active RasV12 and active c-Raf. |
Co-immunoprecipitation (RanBPM-c-Raf complex), Hsp90 binding assay, siRNA/shRNA knockdown, ERK phosphorylation assay, Bcl-2 western blot, cell proliferation and migration assays |
PloS one |
Medium |
23118896
|
| 2013 |
RanBP9 physically interacts with tumor suppressor p73, increases endogenous p73alpha levels at both transcriptional and post-translational levels, and cooperates with p73 to induce mitochondria-mediated cell death (loss of mitochondrial membrane potential, Bax oligomerization, cytochrome c release); RanBP9 knockdown suppresses p73-induced apoptosis and vice versa. |
Co-immunoprecipitation, p73 western blot (transcriptional and stability analysis), siRNA knockdown of p73 and RanBP9, mitochondrial membrane potential assay, Bax oligomerization, cytochrome c release, Mdivi-1/Bcl-2/Bcl-xl inhibitor experiments |
Cell death & disease |
High |
23348590
|
| 2013 |
RanBP9 potentiates Abeta-induced ROS overproduction, apoptosis, and calcium deregulation in hippocampal neurons; RanBP9 selectively delays cytosolic Ca2+ clearance by the mitochondrial calcium uniporter through cofilin translocation to mitochondria; RanBP9 retards anterograde axonal transport of mitochondria and decreases synaptic mitochondrial activity. |
Primary hippocampal neuron overexpression, ROS assay, Ca2+ imaging, mitochondrial calcium uniporter blockade, cofilin mitochondrial translocation assay, axonal transport live imaging |
FASEB journal |
Medium |
23982146
|
| 2013 |
COPS5 (Jab1/CSN5) is a novel RanBP9-interacting protein that stabilizes RanBP9 protein levels, thereby increasing Abeta generation; COPS5 increases RanBP9 half-life; COPS5 knockdown reduces Abeta generation. |
Yeast two-hybrid (human brain library), co-immunoprecipitation in neuronal and non-neuronal cells and mouse brain, protein half-life assay, siRNA knockdown, Abeta ELISA |
The Journal of biological chemistry |
Medium |
23926111
|
| 2013 |
RanBPM interacts with TRAF6 via its SPRY motif; RanBPM inhibits TRAF6 ubiquitination and suppresses TRAF6-triggered NF-κB signaling; RanBPM also blocks TGF-β-induced TβRI nuclear accumulation by competing with TRAF6 for TβRI binding. |
Yeast two-hybrid, GST pull-down, co-immunoprecipitation, confocal microscopy, FRET, ubiquitination assay, NF-κB reporter assay |
Cellular signalling |
Medium |
24103590
|
| 2014 |
RanBPM promotes aggresome formation: ionizing radiation and proteasome inhibition cause RanBPM redistribution into perinuclear aggresomes with ubiquitin, dynein, and HDAC6; aggresome formation by HDAC6 is markedly impaired in RanBPM shRNA cells but restored by RanBPM re-expression; RanBPM interacts with HDAC6 via its LisH/CTLH domain and inhibits HDAC6 deacetylase activity. |
Immunofluorescence for aggresome markers, shRNA knockdown with rescue, co-immunoprecipitation (RanBPM-HDAC6), deacetylase activity assay, LisH/CTLH deletion mutant analysis |
Biology open |
High |
24795145
|
| 2014 |
AXL, LRP-1, and RANBP9 form a multiprotein complex mediating DC efferocytosis; AXL binds apoptotic cells but requires LRP-1 for internalization; RANBP9 bridges AXL and LRP-1 (which do not interact directly) to form the complex; this complex is required for DC antigen cross-presentation to CD8+ T cells; mice lacking DC-specific LRP-1, AXL, or RANBP9 show increased AC accumulation and defective viral antigen-specific T cell responses. |
Targeted genetic deletion in mice, spleen efferocytosis assay, co-immunoprecipitation (AXL-RANBP9-LRP1), DC-T cell coculture cross-presentation assay, HSV-1 infection model |
The Journal of clinical investigation |
High |
24509082
|
| 2014 |
RanBP9 physically interacts with tau and Hsp90/Hsc70 chaperone complexes; RanBP9 overexpression or knockdown directly increases or reduces tau levels in vitro and in vivo; RanBP9 enhances Hsp90 and Hsc70 ATPase activities; genetic reduction of RanBP9 ameliorates tauopathy in Tau-P301S mice. |
Co-immunoprecipitation (RanBP9-tau-Hsp90/Hsc70), in vitro ATPase assay, RanBP9 overexpression/knockdown western blot, Tau-P301S mouse model genetic reduction |
Human molecular genetics |
High |
29016855
|
| 2015 |
RanBP9 interacts with HDAC6 and, together with the CTLH complex (via Twa1 and MAEA), inhibits HDAC6 deacetylase activity toward alpha-tubulin; RanBPM associates with microtubules in an HDAC6-dependent manner; RanBPM knockdown-induced increase in cell migration is due to relief of HDAC6 inhibition. |
Co-immunoprecipitation of HDAC6 with CTLH complex members, acetylated alpha-tubulin western blot, confocal microscopy, shRNA knockdown of multiple CTLH members, wound-healing migration assay |
BMC cancer |
Medium |
28668087
|
| 2015 |
RanBPM contains two distinct nuclear localization motifs (N-terminal proline/glutamine-rich region dominant; C-terminal contributes minimally), one nuclear export signal (NES) whose mutation prevents cytoplasmic accumulation, and its cytoplasmic localization is also conferred by protein-protein interactions; in the cytoplasm, RanBPM partially co-localizes with and associates with alpha-tubulin; in the nucleus, RanBPM is associated with chromatin. |
Systematic deletion mutant analysis in RanBPM shRNA background, confocal microscopy, microtubule co-localization, chromatin fractionation |
PloS one |
Medium |
25659156
|
| 2015 |
Endogenous RanBP9 mediates Abeta-induced cofilin translocation to mitochondria via Slingshot homolog 1 (SSH1); RanBP9 positively regulates SSH1 levels; RanBP9 reduction in APP/PS1 mice protects against cofilin-actin pathology, synaptic damage, gliosis, and Abeta accumulation; RanBP9 reduction significantly enhances LTP and partially rescues contextual memory deficits. |
siRNA knockdown, primary neuron cofilin translocation assay, in vivo APP/PS1 mouse RanBP9 reduction, LTP electrophysiology, behavioral memory testing |
Cell death & disease |
High |
25741591
|
| 2016 |
Ran Binding Protein 9 (RanBP9) is phosphorylated by active ATM on at least S181 and S603 in response to ionizing radiation; DNA damage promotes RanBP9 nuclear accumulation in an ATM-dependent manner; RanBP9 silencing causes delayed activation of ATM, Chk2, γH2AX, and p53, and reduces homologous recombination efficiency, leading to enhanced IR-induced senescence and apoptosis. |
ATM phosphorylation site identification (S181/S603), ATM inhibition experiments, nuclear accumulation assay, RanBP9 stable silencing in multiple cell lines, ATM/Chk2/γH2AX western blot, homologous recombination reporter assay |
Oncotarget |
High |
26943034
|
| 2016 |
RanBPM/RanBP9 scaffold protein binds c-Kit receptor tyrosine kinase and is required for normal c-Kit protein expression in mouse testis and hematopoietic lineages; RanBPM deletion reduces c-Kit protein but not mRNA, indicating post-translational regulation; this regulation is specific to c-Kit among membrane proteins examined. |
Co-immunoprecipitation (RanBPM-c-Kit), western blot (protein vs mRNA comparison), RanBPM-null mice phenotypic analysis, human cell line endogenous expression analysis |
Oncotarget |
Medium |
27835883
|
| 2016 |
Crystal structure of the IUS-SPRY domain of RanBPM was determined; this domain adopts a beta-sandwich fold with a unique shallow binding surface formed by conserved loops, positive patch, and a tryptophan-lined bottom; a 20-mer peptide of DDX-4 (RNA helicase) binds this surface with KD ~13 µM; mutagenesis studies elucidate the interaction interface. |
X-ray crystallography of SPRY domain, crystal structure of peptide-domain complex, isothermal titration calorimetry or equivalent binding assay (KD determination), site-directed mutagenesis |
Journal of molecular biology |
High |
27622290
|
| 2016 |
RanBP9 SPRY domain interacts with TSSC3 PH domain; RanBP9/TSSC3 complex forms a ternary complex with Src, scaffolding their interaction; this suppresses Src and Src-dependent Akt pathway activation, facilitating mitochondrial-associated anoikis and suppressing lung metastasis in vivo. |
Co-immunoprecipitation (RanBP9-TSSC3-Src), domain mapping, anoikis assay, Src/Akt phosphorylation western blot, in vivo lung metastasis model |
Cell death & disease |
Medium |
28032865
|
| 2017 |
CLOCK interacts with RANBP9 (confirmed by yeast two-hybrid and co-immunoprecipitation in mouse testis); RANBP9 previously known to interact with SF3B3 (spliceosome component); CLOCK also interacts with SF3B3; CLOCK binds mRNAs involved in spermatogenesis (demonstrated by RIP-Seq), suggesting CLOCK-RANBP9 involvement in alternative splicing. |
Yeast two-hybrid, co-immunoprecipitation in mouse testis, RIP-Seq |
Gene |
Low |
29126923
|
| 2023 |
RanBP9 physically interacts with p21 and recruits the deubiquitinase USP11 to maintain p21 protein stability by deubiquitination; RanBP9 silencing decreases p21 protein levels whereas overexpression increases p21 independent of p53 status; DNA damage promotes nuclear translocation of RanBP9 via ATM signaling; RanBP9 regulates DDR in a p21-dependent manner. |
Co-immunoprecipitation (RanBP9-p21-USP11), in vivo ubiquitylation assay, RanBP9 overexpression/silencing, nuclear translocation assay with ATM inhibition, DDR functional assays |
Cellular oncology |
Medium |
37676377
|
| 2025 |
In lung macrophages, RanBP9-V5 co-immunoprecipitates known CTLH complex members; however, >90% of the lung RanBP9-associated proteome differs between the two tagged versions (V5 vs HA), revealing macrophage-specific interactions with proteins involved in innate immune response, DNA damage response, metabolism, and mitochondrial function. |
In vivo knock-in mouse model (RanBP9-TurnX with LysM-Cre), tandem affinity immunoprecipitation with mass spectrometry from lung tissue |
Cell death discovery |
Medium |
40223093
|
| 2025 |
RANBP9 and RANBP10 can each independently support CTLH complex formation; acute overexpression of either Scorpin reshapes the NSCLC cell proteome and ubiquitylome; higher RANBP9/RANBP10 ratio is associated with greater cell proliferation; they act as partial antagonists modulating the CTLH complex ubiquitylation output. |
Inducible overexpression/loss-of-function cell lines, proteomics, ubiquitylome profiling, patient tumor lysate analysis |
Journal of experimental & clinical cancer research |
Medium |
40883813
|