Affinage

Showing CLIP1 — CLIP-170 is a alias.

CLIP1

CAP-Gly domain-containing linker protein 1 · UniProt P30622

Length
1438 aa
Mass
162.2 kDa
Annotated
2026-06-09
100 papers in source corpus 49 papers cited in narrative 49 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CLIP1 (CLIP-170) is a homodimeric microtubule plus-end tracking protein (+TIP) that links growing microtubule ends to organelle capture, minus-end-directed transport, and microtubule dynamics regulation (PMID:1356075, PMID:10052454, PMID:19758557). It is a thin 135-nm homodimer in which a long coiled-coil rod connects an N-terminal microtubule/tubulin-binding region — built from tandem CAP-Gly modules, with the second CAP-Gly domain and adjacent serine-rich region constituting the minimal plus-end tracking and polymerization-promoting unit — to a C-terminal cargo/metal-binding domain (PMID:1356075, PMID:10464331, PMID:16120651). Plus-end tracking is not autonomous: CLIP-170 alone diffuses on the lattice, and EB1 is necessary and sufficient to confer end-specificity, with CLIP-170 recognizing composite sites formed by end-accumulated EB1 and tyrosinated α-tubulin through multivalent CAP-Gly and SXIP-like modules (PMID:19126680, PMID:19103809, PMID:30455356). At the plus end CLIP-170 promotes microtubule rescue and nucleation via curved tubulin-oligomer intermediates and, with EB1, cooperatively tunes the stabilizing GTP cap (PMID:15589150, PMID:22424550). Through its C-terminal zinc-finger motifs, CLIP-170 recruits dynactin (p150Glued) and binds LIS1, which together couple it to cytoplasmic dynein; p150Glued and LIS1 compete for the same C-terminal site, and an intramolecular fold between the N- and C-termini autoinhibits microtubule binding (PMID:11940666, PMID:12789661, PMID:15381688). This +TIP-to-dynein relay drives capture of membrane organelles at growing ends and initiation of retrograde transport — of melanosomes, EGFR- and Met-containing endosomes, and incoming herpesvirus particles — and positions CLIP-170 at unattached kinetochores where it supports chromosome congression, kinetochore-microtubule attachment, and PLK1 recruitment during mitosis (PMID:16362039, PMID:19758557, PMID:25413345, PMID:26504169, PMID:30537020, PMID:24777477). CLIP-170 activity is extensively controlled by phosphorylation: mTOR, AMPK, JNK, CDK1, Plk1, CK2, and LRRK1 phosphorylate distinct sites to regulate its microtubule affinity, rescue activity, dynactin/dynein engagement, and kinetochore function, governing directional cell migration, cardiomyocyte microtubule turnover, and MTOC repositioning (PMID:12231510, PMID:20495555, PMID:32491151, PMID:20664522, PMID:24451569, PMID:25413345, PMID:33251722). CLIP-170 also coordinates microtubule-actin cross-talk through direct, mutually exclusive binding to F-actin and via IQGAP1 and the formin mDia1, supporting cell polarization, dendrite morphology, phagocytosis, and non-centrosomal MTOC assembly (PMID:35283190, PMID:12110184, PMID:19114595, PMID:21430156, PMID:28179500), and negatively regulates TLR4 signaling by promoting ubiquitination and degradation of the adaptor TIRAP (PMID:29222167). Genetic knockout establishes that CLIP-170 is essential for spermatogenesis and male fertility (PMID:16230537).

Mechanistic history

Synthesis pass · year-by-year structured walk · 24 steps
  1. 1992 High

    Established CLIP-170 as the founding molecular linker between membranous organelles and microtubules, defining the modular architecture that all later mechanism rests on.

    Evidence cDNA cloning, in vitro vesicle-microtubule binding assay, and domain analysis

    PMID:1356075

    Open questions at the time
    • Did not define how plus-end specificity arises
    • C-terminal cargo partners not yet identified
  2. 1994 High

    Mapped the division of labor between domains — N-terminal tandem repeat for microtubule binding and C-terminal domain for peripheral cargo anchoring — converting the structural model into a functional one.

    Evidence Domain/deletion mutant expression in HeLa and Vero cells with immunofluorescence

    PMID:7983157

    Open questions at the time
    • Mechanism of end-tracking vs lattice binding unresolved
    • No direct partner identification
  3. 1999 High

    Discovered that CLIP-170 treadmills on growing plus ends coupled to active polymerization and biochemically characterized the homodimer and its tubulin/plus-end binding, establishing the +TIP behavior and its link to newly polymerized tubulin.

    Evidence GFP live-cell imaging, biotin-tubulin tracing, in vitro co-sedimentation/cross-linking, and EM of purified protein

    PMID:10052454 PMID:10464331 PMID:9885247

    Open questions at the time
    • Whether end-tracking is autonomous or requires partners unknown
    • Binding stoichiometry to dimer vs polymer not fully resolved
  4. 1999 Medium

    Placed CLIP-170 upstream of dynactin at plus ends, linking +TIP behavior to the dynein transport machinery for endosomal cargo loading.

    Evidence Colocalization and overexpression of WT/mutant CLIP-170 and p150Glued with endosomal trafficking assays

    PMID:10212138 PMID:10588646

    Open questions at the time
    • Direct binding site not yet mapped
    • Overexpression-based; physiological requirement unestablished
  5. 1998 Medium

    Identified CLIP-170 at prometaphase kinetochores codistributing with dynein/dynactin, extending its role from interphase trafficking to mitotic chromosome segregation.

    Evidence Immunofluorescence, C-terminal fragment and dynamitin overexpression

    PMID:9585405

    Open questions at the time
    • Targeting mechanism inferred from dynamitin, not directly demonstrated
    • Functional contribution to attachment not yet tested by depletion
  6. 2002 High

    Mapped the C-terminal zinc-finger to LIS1 and dynactin binding and connected CLIP-170 to Rac1/Cdc42-IQGAP1 signaling, defining how it couples to dynein and to actin-based polarity cues.

    Evidence Reciprocal Co-IP, two-hybrid, domain mutagenesis, and live imaging in cells

    PMID:11889140 PMID:11940666 PMID:12110184

    Open questions at the time
    • How LIS1/dynactin binding is coordinated in time unclear
    • Direct vs indirect IQGAP1 contact at residue level not defined
  7. 2002 High

    Showed mTOR directly phosphorylates CLIP-170 to positively regulate its microtubule binding, opening the theme of kinase control of +TIP activity.

    Evidence Co-IP, in vitro kinase assay, rapamycin treatment, and microtubule-binding assay

    PMID:12231510

    Open questions at the time
    • Phospho-sites not mapped
    • In vivo physiological context undefined
  8. 2004 High

    Resolved how CLIP-170 modulates dynamics and how its own activity is gated — promoting rescue/nucleation via curved tubulin oligomers while an intramolecular fold autoinhibits microtubule binding and sets up p150Glued/LIS1 competition.

    Evidence In vitro dynamics assay, cryo-EM, scanning force microscopy, FRET, RNAi, and direct binding assays

    PMID:15381688 PMID:15589150

    Open questions at the time
    • What relieves autoinhibition in vivo not established here
    • Structural basis of oligomer induction at atomic resolution lacking
  9. 2005 High

    Defined the minimal plus-end tracking unit (second CAP-Gly + serine-rich region) and CLIP-170's preference for GTP-tubulin dimer, and demonstrated its functional requirement at kinetochores for chromosome congression.

    Evidence In vitro biochemistry, live-cell domain imaging, and RNAi with mitotic readouts

    PMID:16120651 PMID:16362039

    Open questions at the time
    • Kinetochore study Medium confidence, single lab
    • How GTP-tubulin discrimination is achieved structurally unclear
  10. 2005 High

    Demonstrated genetically that CLIP-170 is essential for male fertility and undergoes a +TIP-to-structural transition in spermatids, establishing an organismal, non-trafficking role.

    Evidence Knockout and GFP knock-in mice, live testis imaging, and FRAP

    PMID:16230537

    Open questions at the time
    • Molecular basis of the mobility transition unknown
    • Manchette/centrosome binding partners in spermatids unidentified
  11. 2008 High

    Resolved the long-standing question of plus-end specificity: in vitro single-molecule reconstitution showed EB1 is necessary and sufficient for CLIP-170 end-tracking, which depends on EB1 plus tyrosinated α-tubulin and GTP hydrolysis, not motor activity.

    Evidence TIRF single-molecule reconstitution with purified proteins and GMPCPP/tyrosination controls

    PMID:18283108 PMID:19103809 PMID:19126680

    Open questions at the time
    • How EB1 dependence integrates with intrinsic tubulin affinity in cells unclear
    • Stoichiometry of the composite binding site not fully defined
  12. 2008 High

    Extended CLIP-170 function into innate immunity, spindle bipolarity, and actin regulation — direct mDia1 binding for phagocytosis, dynein-dependent counteraction of Eg5, and CR3-triggered actin polymerization.

    Evidence RNAi, dominant-negative expression, direct binding assays, and phagocytosis/spindle assays

    PMID:19020519 PMID:19114595

    Open questions at the time
    • mDia1 binding interface not residue-mapped
    • Eg5-counteraction study Medium confidence
  13. 2009 High

    Demonstrated CLIP-170 initiates minus-end-directed organelle transport by capturing cargo at growing plus ends, and that it contacts both α- and β-tubulin H12 helices, mechanistically linking +TIP capture to dynein transport.

    Evidence Live melanophore imaging with MT-dynamics inhibition, plus cross-linking/mass spectrometry of tubulin contacts

    PMID:19758557 PMID:19913027

    Open questions at the time
    • Handoff step from CLIP-170 capture to dynein motility not directly visualized
    • Tubulin contact study Medium confidence
  14. 2009 Medium

    Initiated the cell-cycle kinase control theme by showing CDK1/Cdc2 phosphorylates CLIP-170 at Thr287 to control localization, mitotic progression, and prevention of centrosome reduplication.

    Evidence Co-IP, in vivo phosphorylation assay, T287A mutant expression, and centrosome counting

    PMID:19687009

    Open questions at the time
    • Single lab; downstream effector of T287 phosphorylation initially unclear
    • Mechanism of centrosome reduplication suppression not detailed
  15. 2010 High

    Established a multi-kinase phospho-code: AMPK controls CLIP-170-dependent MT dynamics and directional migration, while Plk1 (S195) and CK2 (S1318) jointly govern dynactin binding and kinetochore-MT attachment timing.

    Evidence In vitro kinase assays, phospho-site mapping, phosphomimetic rescue, and migration/kinetochore-fiber assays

    PMID:20495555 PMID:20664522

    Open questions at the time
    • How distinct phosphorylations are spatiotemporally integrated unclear
    • Phosphatases reversing these marks not identified
  16. 2011 High

    Connected CLIP-170 to neuronal morphogenesis and clarified the EB1-CLIP-170 cooperative mechanism on dynamics: mTOR-promoted CLIP-170/IQGAP1 complex shapes dendrites, and EB1+CLIP-170 deplete end-bound Pi to modify the GTP cap.

    Evidence Co-IP, RNAi, dendrite morphometry, and in vitro dynamics with SAXS/AUC/[γ-32P]GTP pulsing

    PMID:21430156 PMID:22424550

    Open questions at the time
    • Dendrite study Medium confidence
    • Link between GTP-cap modification and rescue in cells not established
  17. 2013 High

    Identified a direct small-molecule regulator: pregnenolone binds the coiled-coil to switch CLIP-170 to an extended active conformation, increasing MT, dynactin, and LIS1 engagement — a non-kinase route to relieving autoinhibition.

    Evidence Photoaffinity capture, direct binding, conformational analysis, zebrafish epiboly, and migration assays

    PMID:23955365

    Open questions at the time
    • Physiological pregnenolone concentrations and tissue relevance unclear
    • Binding site not residue-resolved
  18. 2014 High

    Defined the mitotic phospho-network in detail — CDK1-T287 enables PLK1 kinetochore recruitment, Plk1-S312 cyclically tunes MT-end binding, and LRRK1-T1384 promotes dynein-dynactin engagement for EGFR endosome transport.

    Evidence In vitro kinase/binding assays, site mapping, phosphomutant rescue, and kinetochore/transport assays

    PMID:24451569 PMID:24777477 PMID:25413345

    Open questions at the time
    • Order of these phospho-events within mitosis not fully resolved
    • Cross-talk between LRRK1 and cell-cycle kinases unexplored
  19. 2015 High

    Demonstrated that CLIP-170 captures incoming herpesvirus particles in an EB1/DCTN1 +TIP complex to initiate retrograde transport, distinguishing CLIP-170-specific from general dynein function.

    Evidence RNAi, dominant-negative expression, live imaging, and quantitative infection assay in primary human cells

    PMID:26504169

    Open questions at the time
    • Direct viral-capsid contact not biochemically defined
    • Whether all retrograde cargoes use the same capture mode unclear
  20. 2016 High

    Quantified how CLIP-170 phosphorylation and α-tubulin tyrosination jointly time and probabilistically gate initiation of dynein-driven retrograde transport in axons.

    Evidence Single-molecule reconstitution, neuronal transport assays, and computational simulation

    PMID:26972003

    Open questions at the time
    • Which kinase sets the relevant phospho-state in the distal axon unspecified here
    • In vivo relevance to axonal cargoes broadly not tested
  21. 2017 High

    Showed CLIP-170 (with IQGAP1/Rac1) drives ninein redeployment to non-centrosomal MTOCs during epithelial differentiation, and identified TIRAP degradation as a mechanism for CLIP-170 negative regulation of TLR4 inflammation.

    Evidence RNAi, double-KO mouse tissue/organoids, immunofluorescence; and Co-IP, ubiquitination assay, cytokine ELISA, in vivo siRNA

    PMID:28179500 PMID:29222167

    Open questions at the time
    • TLR4/TIRAP study Medium confidence
    • Mechanism by which CLIP-170 promotes TIRAP ubiquitination (E3 identity) unknown
  22. 2018 High

    Resolved the molecular basis of EB1 engagement and added immune cell function: multivalent CAP-Gly/SXIP-like modules strengthen EB1 binding, and AMPK-phosphorylated CLIP-170 is required for MTOC repositioning to the immune synapse.

    Evidence ITC, SEC, mutagenesis; and imaging with phosphomutant/dominant-negative AMPK plus dynein single-molecule tracking

    PMID:30455356 PMID:30487641

    Open questions at the time
    • Immune-synapse study Medium confidence
    • How multivalency is regulated dynamically in cells unclear
  23. 2020 High

    Added JNK as a stress-activated regulator boosting CLIP-170 rescue activity, and established AMPK-S311 phosphorylation as a physiological controller of cardiomyocyte microtubule turnover.

    Evidence In vitro kinase/dynamics assays with phosphomutants; and S311A transgenic mice with cardiac imaging and pharmacology

    PMID:32491151 PMID:33251722

    Open questions at the time
    • Relationship between S311 (AMPK) and other AMPK sites unclear
    • How rescue remnants are selected as future rescue sites unresolved
  24. 2021 High

    Expanded the CLIP-170 interactome and properties: direct mutually exclusive F-actin/MT binding, recycling Met-endosome transport, anti-inflammatory SOCS3 and TFPI2/TIRAP axes, DCTN1 competition restraining HIV-1 infection, and condensate-like phase behavior.

    Evidence Co-sedimentation/competition, Co-IP, live imaging, ubiquitination assays, infectivity assays, KO/KD models, and FRAP

    PMID:30537020 PMID:33372035 PMID:34686593 PMID:34890409 PMID:35283190 PMID:39617791

    Open questions at the time
    • Several axes (Met, SOCS3, TFPI2, HIV-1, condensate) are Medium confidence single-lab
    • Physiological significance of CLIP-170 phase separation undefined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple kinase inputs, conformational switching, EB1-dependent tracking, and competing C-terminal partners are integrated to dictate cargo specificity in a given cellular context remains unresolved.
  • No unified model linking phospho-state to choice of cargo or pathway
  • Phosphatases and the in vivo trigger relieving autoinhibition largely unidentified
  • Functional role of phase separation versus discrete complexes unclear

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 4 GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3
Localization
GO:0005815 microtubule organizing center 3 GO:0005856 cytoskeleton 3 GO:0000228 nuclear chromosome 2 GO:0005829 cytosol 2
Pathway
R-HSA-1640170 Cell Cycle 5 R-HSA-5653656 Vesicle-mediated transport 4 R-HSA-162582 Signal Transduction 3 R-HSA-168256 Immune System 3
Partners
DCTN1EB1IQGAP1LIS1MDIA1MTORSOCS3TIRAP
Complex memberships
EB1/CLIP-170 +TIP networkRac1/Cdc42-IQGAP1-CLIP-170 complexdynein-dynactin complex

Evidence

Reading pass · 49 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 CLIP-170 links endocytic carrier vesicles to microtubules in vitro; its N-terminal domain contains a novel tandem-repeat motif responsible for microtubule binding, and the protein forms a homodimer with a long central coiled-coil domain connecting the N-terminal microtubule-binding domain to the C-terminal organelle-interacting domain. cDNA cloning, in vitro vesicle-microtubule binding assay, domain analysis Cell High 1356075
1994 The tandem repeat in the N-terminal domain of CLIP-170 is essential for microtubule binding in vivo; the C-terminal domain is required for anchoring microtubules to peripheral cytoplasmic structures (cargo-binding function), and overexpression of intact CLIP-170 causes microtubule bundling dependent on the C-terminal domain. Transient expression of intact and deletion/mutation mutants in HeLa and Vero cells, immunofluorescence Journal of cell science High 7983157
1999 CLIP-170 dynamically treadmills on growing microtubule plus ends in vivo at rates matching microtubule elongation (~0.15–0.4 µm/s), highlighting newly polymerized tubulin; microtubule-drug treatment rapidly abolishes this movement, indicating that plus-end association is coupled to active polymerization. GFP-CLIP-170 live-cell imaging, fluorescent speckle microscopy, pharmacological perturbation Cell High 10052454
1999 CLIP-170 plus-end targeting is closely linked to tubulin polymerization: the N-terminal microtubule-interacting domain alone localizes to plus ends; CLIP-170 associates with newly formed microtubules traced by biotinylated tubulin and cross-links/sediments with non-polymerized tubulin in vitro. Biotin-tubulin microinjection, in vitro co-sedimentation, cross-linking, transfection of domain fragments The Journal of cell biology High 9885247
1999 CLIP-170 recruits dynactin to microtubule plus ends via its C-terminal putative cargo-binding domain; overexpression of p150(Glued) and mutant CLIP-170 forms indicate that CLIP-170 is upstream of dynactin in endosomal cargo loading at microtubule ends. Colocalization immunofluorescence, overexpression of wild-type and mutant CLIP-170 and p150(Glued), endosomal trafficking assays Molecular biology of the cell Medium 10588646
1999 Dynactin and CLIP-170 colocalize along distal segments of interphase microtubules; dynactin (Arp1 subunit) can be removed from microtubules by dynamitin overexpression without affecting CLIP-170, indicating they use partially distinct microtubule-association mechanisms. Multi-antibody immunofluorescence, dynamitin overexpression, temperature-shift experiments Journal of cell science Medium 10212138
1999 CLIP-170 is a thin 135-nm homodimer with two kinks in its coiled-coil rod; the N-terminal domain binds microtubules with a stoichiometry of one dimeric head per four tubulin heterodimers; the rod and tail domains reduce microtubule-binding stoichiometry of the full-length protein. Purification of authentic CLIP-170, electron microscopy (glycerol spray/rotary shadowing), in vitro microtubule-binding stoichiometry assays The Journal of biological chemistry High 10464331
1998 CLIP-170 transiently localizes to prometaphase kinetochores and codistributes with dynein and dynactin there; overexpression of the C-terminal domain displaces endogenous CLIP-170 from kinetochores and causes a prometaphase delay; dynamitin overexpression reduces CLIP-170 at kinetochores, suggesting dynein/dynactin-dependent kinetochore targeting of CLIP-170. Immunofluorescence, transient overexpression of C-terminal CLIP-170 fragment, dynamitin overexpression The Journal of cell biology Medium 9585405
2002 IQGAP1 (an effector of Rac1/Cdc42) directly interacts with CLIP-170, and activated Rac1/Cdc42, IQGAP1, and CLIP-170 form a tripartite complex. Expression of C-terminal IQGAP1 fragment (containing the CLIP-170 binding region) delocalizes GFP-CLIP-170 from microtubule tips and alters microtubule arrays; IQGAP1 mutant defective in Rac1/Cdc42 binding induces multiple leading edges. Co-immunoprecipitation, pulldown, GFP live imaging, dominant-negative overexpression in Vero cells Cell High 12110184
2002 CLIP-170 directly interacts with LIS1 via the distal zinc finger motif of CLIP-170's C-terminal domain; LIS1 is required for CLIP-170 kinetochore recruitment, and LIS1 acts as a regulated adapter between CLIP-170 and cytoplasmic dynein. Overexpression of CLIP-170 causes zinc finger-dependent co-localization of phospho-LIS1 and dynactin on microtubule bundles. Co-immunoprecipitation, colocalization, domain mutant overexpression, indirect immunofluorescence Molecular and cellular biology High 11940666
2002 LIS1 WD-repeat domain overexpression displaces CLIP-170 from kinetochores without affecting dynein/dynactin; LIS1 NH2-terminal overexpression displaces endogenous LIS1 with no effect on CLIP-170, dynein, or dynactin; dynamitin overexpression removes both CLIP-170 and LIS1. LIS1 interacts directly with dynein heavy chain (AAA1 domain) and intermediate chain, and with dynamitin. Co-expression/co-immunoprecipitation, two-hybrid assay, domain overexpression, immunofluorescence The Journal of cell biology High 11889140
2002 FRAP/mTOR interacts with CLIP-170 and phosphorylates it in vitro at rapamycin-sensitive sites; rapamycin inhibits CLIP-170 binding to microtubules in vivo, indicating that mTOR-mediated phosphorylation positively regulates CLIP-170 microtubule-binding activity. Co-immunoprecipitation, in vitro kinase assay, rapamycin treatment, microtubule-binding assay EMBO reports High 12231510
2003 CLIP-170 interacts with dynactin via the second metal-binding (zinc finger) motif of its C-terminal tail, and with EB1 via a mechanism requiring neither metal-binding motif; these interactions are separable, and CLIP-170 can target dynactin to microtubule plus ends independently of EB1. Site-directed mutagenesis, transfection/colocalization assay in mammalian cells Cell motility and the cytoskeleton Medium 12789661
2004 CLIP-170 N-terminal domain (H2) promotes microtubule rescues and stimulates nucleation in vitro; by cryo-EM, H2 induces tubulin ring formation in solution and curved oligomers at microtubule plus ends, suggesting CLIP-170 copolymerizes with tubulin and modulates dynamics through tubulin-oligomer intermediates. In vitro microtubule dynamics assay (pure tubulin + centrosomes), electron cryomicroscopy Current biology : CB High 15589150
2004 CLIP-170 undergoes an intramolecular autoinhibitory interaction between its N-terminal microtubule-binding domain (first metal-binding motif) and its C-terminal domain, as shown by scanning force microscopy and FRET. This intramolecular folding reduces MT-binding. The NH2 terminus of p150(Glued) binds the CLIP-170 C-terminus (second metal-binding motif); p150(Glued) and LIS1 compete for binding to the CLIP-170 C-terminus. RNAi depletion of CLIP-170 strongly reduces dynactin accumulation at MT tips. Scanning force microscopy, FRET, RNAi knockdown, direct binding assays (GST pulldown/co-IP), immunofluorescence The Journal of cell biology High 15381688
2005 CLIP-170 has stronger affinity for tubulin dimer than polymer and can distinguish GTP- from GDP-tubulin; the second CAP-Gly domain with adjacent serine-rich region is the minimal plus-end tracking unit capable of both +TIP behavior in vivo and tubulin polymerization promotion in vitro, whereas the first CAP-Gly domain alone is incompetent for either activity. In vitro biochemistry (sedimentation, affinity assays), live-cell imaging of CLIP-170 CAP-Gly domain fragments Molecular biology of the cell High 16120651
2005 CLIP-170 localizes dynamically to the outermost part of unattached kinetochores and to growing microtubule ends; RNAi depletion of CLIP-170 causes defective chromosome congression and diminished kinetochore-microtubule attachments without detectably affecting microtubule dynamics or k-fiber stability. High-resolution immunofluorescence, RNAi depletion, live-cell imaging The EMBO journal Medium 16362039
2005 CLIP-170 is essential for male fertility and spermatogenesis; in spermatids it associates with the manchette and centrosomes and transitions from a mobile plus-end tracking protein to a relatively immobile structural protein, indicating a structural role in spermatid differentiation and sperm head shaping. CLIP-170 knockout and GFP knock-in mice, live testis imaging, FRAP Genes & development High 16230537
2006 EB1 is required for plus-end localization of CLIP-170, which in turn is required to localize p150(Glued) to plus ends; CLIP-170 depletion causes defects in microtubule dynamics and cell polarization after scratch wounding. However, removal of p150(Glued) from plus ends by EB1 or CLIP-170 depletion does not affect organelle distribution or membrane traffic, indicating that CLIP-170/p150(Glued) plus-end function is not required for general membrane trafficking. RNAi depletion (EB1, CLIP-170, p150Glued), immunofluorescence, membrane trafficking assays (transferrin uptake, ER-Golgi transport), live-cell imaging Journal of cell science High 16772339
2008 CLIP-170 requires EB1 for microtubule plus-end tracking; reconstituted in vitro at single-molecule resolution, EB1 autonomously tracks growing ends while CLIP-170 alone shows lattice diffusion and fails to selectively track ends. EB1 addition is both necessary and sufficient to mediate CLIP-170 plus-end tracking. GTP hydrolysis is required for end-specificity. In vitro reconstitution with TIRF single-molecule microscopy, pharmacological (GMPCPP) perturbation Proceedings of the National Academy of Sciences of the United States of America High 19126680
2008 EB1 autonomously recognizes specific binding sites at growing microtubule ends; CLIP-170 does not end-track by itself but requires EB1 and recognizes composite binding sites constituted by end-accumulated EB1 and tyrosinated α-tubulin; unlike fission yeast Tip1, mammalian CLIP-170 end-tracking does not require motor activity. In vitro reconstitution with purified proteins, TIRF microscopy, tubulin tyrosination manipulation The Journal of cell biology High 19103809
2008 GFP-CLIP-170 turns over rapidly on microtubule plus ends (rate-limited by diffusion); growing microtubule ends contain a surplus of relatively low-affinity CLIP-170 binding sites. The apparent comet fluorescence loss does not reflect single-molecule behavior but overall structural changes at the MT end. Quantitative fluorescence microscopy, FRAP, single-molecule analysis of GFP-CLIP-170 and GFP-EB3 The Journal of cell biology Medium 18283108
2008 CLIP-170 is specifically required for efficient CR3/αMβ2-integrin-triggered phagocytosis in macrophages; it directly interacts with the formin homology 2 (FH2) domain of mDia1 via a direct protein-protein interaction, controls mDia1 recruitment to phagocytic cups, and thereby regulates actin polymerization essential for phagocytosis. This interaction is negatively regulated during αMβ2-mediated phagocytosis. RNAi knockdown, dominant-negative expression, direct binding assay, immunofluorescence, phagocytosis assay The Journal of cell biology High 19114595
2008 Dynein, Lis1, and CLIP-170 counteract Eg5-dependent centrosome separation during bipolar spindle assembly; CLIP-170 depletion allows spindle bipolarity with less Eg5 activity, a function mediated through CLIP-170's interaction with dynein (not shared by CLIP-115, which lacks the dynein-dynactin interaction domain). RNAi depletion in human cells, spindle bipolarity assay, Eg5 inhibitor (monastrol) titration The EMBO journal Medium 19020519
2009 CLIP-170 initiates minus-end-directed transport of membrane organelles (melanosomes) in Xenopus melanophores by capturing organelles at growing microtubule plus ends; inhibition of MT dynamics or loss of CLIP-170 from MT tips dramatically inhibits pigment aggregation. Live-cell imaging in Xenopus melanophores, MT dynamics inhibition, CLIP-170 dominant-negative expression Developmental cell High 19758557
2009 CLIP-170 binds to both α-tubulin and β-tubulin (not only the acidic C-terminal tails) including H12 helices of both tubulins, as shown by chemical cross-linking/mass spectrometry. CLIP-170 can use its multiple tubulin-binding sites to bind EB1 and microtubules simultaneously. Chemical cross-linking, mass spectrometry, in vitro binding assays Journal of molecular biology Medium 19913027
2010 AMPK directly phosphorylates CLIP-170; phosphorylation is required for proper microtubule dynamics and directional cell migration. Non-phosphorylatable CLIP-170 causes prolonged MT-tip accumulation and slower tubulin polymerization; these phenotypes are rescued by phosphomimetic CLIP-170. AMPK inhibition impairs MT stabilization and directional migration, also rescued by phosphomimetic CLIP-170. In vitro kinase assay, expression of phosphomimetic/non-phosphorylatable CLIP-170 mutants, live-cell microtubule imaging, cell migration assay (wound healing) Nature cell biology High 20495555
2010 Polo-like kinase 1 (Plk1) phosphorylates CLIP-170 at S195, and casein kinase 2 (CK2) phosphorylates it at S1318; Plk1 phosphorylation enhances CLIP-170 association with CK2; CK2 phosphorylation is required for CLIP-170 interaction with dynactin and kinetochore localization. Both phosphorylation events are required for timely formation of kinetochore-microtubule attachments. In vitro kinase assay, phospho-site mapping, co-immunoprecipitation, expression of phosphomutants, kinetochore-fiber assay The EMBO journal High 20664522
2009 Cdc2 (CDK1) phosphorylates CLIP-170 at Thr287 in vivo; expression of non-phosphorylatable T287A causes CLIP-170 mislocalization, accumulation of Plk1 and cyclin B, and G2/M block; depletion of CLIP-170 leads to centrosome reduplication, and Cdc2 phosphorylation of CLIP-170 is required to prevent it. Co-immunoprecipitation, in vivo phosphorylation assay, T287A phosphomutant expression, centrosome counting, cell cycle analysis The Journal of biological chemistry Medium 19687009
2011 CLIP-170 and IQGAP1 cooperatively regulate dendrite morphology in neurons; mTOR kinase interacts with CLIP-170 and is required for efficient formation of a CLIP-170/IQGAP1 complex; dynamic microtubules, CLIP-170, and IQGAP1 are required for proper dendritic arbor morphology and PI3K-mTOR-induced dendritic complexity. Co-immunoprecipitation, RNAi knockdown, live-cell imaging of dendritic dynamics, morphometric analysis in rat neurons The Journal of neuroscience Medium 21430156
2011 EB1 and a minimal CLIP-170 fragment (ClipCG12 with two non-interacting CAP-Gly domains) cooperatively regulate microtubule dynamic instability; together at 250 nM they modulate dynamics and deplete stably bound Pi at microtubule ends, suggesting they modify the stabilizing GTP cap by cooperative action. In vitro microtubule dynamics assay, SAXS, analytical ultracentrifugation, [γ-32P]GTP pulsing Biochemistry High 22424550
2013 Pregnenolone (P5) directly binds CLIP-170 at its coiled-coil domain, changing it to an extended (active) conformation that increases CLIP-170 interactions with microtubules, dynactin p150(Glued), and LIS1, promoting CLIP-170-dependent microtubule polymerization and cell migration. Photoaffinity probe capture from embryonic extract, direct binding assay, conformational analysis, in vivo zebrafish epiboly assay, mammalian cell migration assay Nature chemical biology High 23955365
2014 CLIP-170 colocalizes with PLK1 at kinetochores during early mitosis; CLIP-170 depletion reduces PLK1 kinetochore recruitment, causing kinetochore-fiber instability and chromosome misalignment. CDK1-dependent phosphorylation at T287 is required: non-phosphorylatable T287A fails to restore PLK1 kinetochore localization or rescue chromosome alignment defects. RNAi depletion, immunofluorescence, phosphomutant (T287A) rescue assay, kinetochore-fiber stability assay Journal of cell science High 24777477
2014 LRRK1 phosphorylates CLIP-170 at Thr1384 in its C-terminal zinc knuckle motif; this promotes CLIP-170 association with dynein-dynactin complexes and causes accumulation of p150(Glued) at microtubule plus ends, thereby facilitating migration of EGFR-containing endosomes. In vitro kinase assay, phospho-site mapping, co-immunoprecipitation, live-cell EGFR trafficking assay Journal of cell science High 25413345
2014 Plk1 phosphorylates CLIP-170 at Ser312 during mitosis; in vitro phosphorylation by Plk1 diminishes CLIP-170 binding to microtubule ends and lattice without affecting EB3 binding; proper Ser312 phosphorylation/dephosphorylation cycling is required for stable kinetochore-microtubule attachment and chromosome alignment. In vitro kinase/binding assay with purified CLIP-170 N-terminal fragment, phospho-site mapping, mitotic phenotype analysis with phosphomutants Cell structure and function High 24451569
2015 CLIP-170 at microtubule plus ends is required to initiate retrograde transport of herpes simplex virus (HSV-1) particles in primary human cells; CLIP-170 functions in a +TIP complex with EB1 and DCTN1 to capture incoming virus particles. Depletion of CLIP-170 completely blocks long-range retrograde transport and suppresses infection ~5000-fold without affecting transferrin uptake or dynein-dependent organelle movement. RNAi depletion, dominant-negative expression, live-cell imaging, infection assay in primary human cells The Journal of cell biology High 26504169
2016 CLIP-170 phosphorylation and α-tubulin tyrosination cooperatively control initiation of dynein-driven retrograde transport in the distal axon; CLIP-170 primarily regulates the time to microtubule encounter, while tyrosination of the lattice regulates the probability of binding. In vitro single-molecule reconstitution, live-cell transport assay in primary neurons, computational simulation, pharmacological manipulation of tubulin PTMs Cell reports High 26972003
2017 CLIP-170 is required for redeployment of ninein from centrosomes to non-centrosomal microtubule organizing centres (n-MTOCs) during epithelial differentiation, thereby enabling apico-basal microtubule array formation; IQGAP1 and active Rac1 cooperate with CLIP-170 in this process. Confirmed using CLIP-170/CLIP-115 double KO intestinal tissue and organoids. RNAi depletion, KO mouse tissue (Clip1/Clip2 double KO), organoid culture, immunofluorescence Open biology High 28179500
2017 CLIP170 interacts with the TLR2/TLR4 adaptor TIRAP, induces its ubiquitination and subsequent proteasomal degradation, and thereby negatively regulates TLR4-mediated proinflammatory cytokine (IL-6, TNF-α) production in macrophages. Co-immunoprecipitation, overexpression/knockdown (siRNA), ubiquitination assay, cytokine ELISA, in vivo siRNA delivery in mice Journal of immunology Medium 29222167
2018 CLIP-170 contains multiple EB1-binding modules in its N-terminal region: two CAP-Gly domains (engaging EB1's C-terminal EEY motif only), a bridging SXIP motif, and an array of divergent SXIP-like motifs N-terminal to the first CAP-Gly domain. These modules act multivalently to strengthen the CLIP-170-EB1 interaction. Isothermal titration calorimetry, size-exclusion chromatography, mutagenesis The Journal of biological chemistry High 30455356
2018 CLIP-170 phosphorylation (by AMPK) is essential for MTOC repositioning to the immunological synapse during T cell activation; T cell stimulation induces dynein co-localization with CLIP-170 and plus-end tracking, and phosphorylated CLIP-170 is required for dynein recruitment to plus-end tracking and subsequent dynein relocation to the contact surface. Fluorescence imaging, CLIP-170 phosphorylation inhibition (dominant-negative AMPK/phosphomutant), single-molecule tracking of dynein Scientific reports Medium 30487641
2019 CLIP-170 associates with MT plus ends to coordinate recycling and outward transport of Met RTK-containing endosomes (Rab4-positive); HGF stimulation induces GGA3 and CLIP-170 recruitment to an activated Met RTK complex, and CLIP-170 is required for net outward movement of Met-positive vesicles toward the cell cortex and lamellipodia. Co-immunoprecipitation, live-cell imaging, dominant-negative CLIP-170, RNAi knockdown, endosome trafficking assay Traffic Medium 30537020
2020 JNK directly phosphorylates CLIP-170 in its microtubule-binding domain upon cell stress, increasing CLIP-170's rescue-promoting activity; phosphomimetic CLIP-170 enhances rescue events in vitro and in cells, and increases CLIP-170 remnant occurrence on the microtubule lattice at potential future rescue sites. In vitro kinase assay, in vitro microtubule dynamics assay, phosphomimetic/non-phosphorylatable mutants, live-cell imaging The Journal of cell biology High 32491151
2020 AMPK-mediated phosphorylation of CLIP-170 at Ser311 regulates microtubule turnover at intercalated disks in cardiomyocytes; inhibition of this phosphorylation (S311A transgenic mice) causes MT accumulation at intercalated disks, cardiomyocyte elongation, and progressive decline in cardiac contraction. CLIP-170 S311A transgenic mouse, time-lapse imaging, pharmacological (MYK-461) modulation of AMPK localization EMBO reports High 33251722
2021 CLIP-170 directly interacts with TIRAP (TLR adaptor) and CLIP-170 induces TIRAP ubiquitination and degradation, negatively regulating TLR4 signaling; TFPI2 inhibits CLIP-170-mediated TIRAP ubiquitination by binding the CLIP-170 R24 residue of TFPI2's KD1 domain, and HOPE (hypothermic oxygenated perfusion) exerts anti-inflammatory effects by modulating the TFPI2/CLIP-170/TIRAP axis. Co-immunoprecipitation, ubiquitination assay, siRNA knockdown, rat liver IRI model, Western blot Experimental & molecular medicine Medium 39617791
2021 DCTN1 (dynactin-1) competes with CLIP-170 for binding to incoming HIV-1 particles; outside its dynactin role, DCTN1 functions as a +TIP that sequesters CLIP-170 from viral cores, inhibiting early HIV-1 infection. Deletion of the zinc knuckle domain of CLIP-170 increases its binding to virus particles but does not promote infection, indicating this Zn domain mediates a critical proviral CLIP-170 function blocked by DCTN1. RNAi knockdown of DCTN1, CLIP-170 Zn-domain deletion mutant, virus particle co-immunoprecipitation, infectivity assay Proceedings of the National Academy of Sciences of the United States of America Medium 34686593
2021 SOCS3 interacts with CLIP-170 (and CLASP2) via its N-terminal domain; the SOCS3-CLIP-170/CLASP2 complex is essential for maximal anti-inflammatory SOCS3 effects in lung endothelium. Knockdown of CLIP-170 impairs SOCS3-JAK2 interaction and abolishes SOCS3's protective effects against IL-6 and bacterial pathogen-induced barrier dysfunction. Co-immunoprecipitation, endothelial cell KD, EC-specific SOCS3 KO mice, lung permeability/inflammation assays The Journal of biological chemistry Medium 33372035
2022 The CLIP-170 N-terminal domain directly binds filamentous actin (F-actin) with relatively weak affinity; the F-actin-binding region overlaps with the microtubule-binding region; in vitro competition assays show that CLIP-170-F-actin and CLIP-170-MT interactions are mutually exclusive. High-speed co-sedimentation assays, CLIP-170 fragment/mutant analysis, in vitro competition assays The Journal of biological chemistry High 35283190
2021 Overexpression of CLIP-170 in cells induces large patch structures with hallmarks of biomolecular condensates (phase-separated liquid droplets): they contain CLIP-170 and other +TIP network proteins, are dynamic by FRAP, and exclude other known condensate markers; bioinformatic analysis confirms conserved intrinsically disordered regions in key +TIPs. Video microscopy, immunofluorescence, FRAP, bioinformatic disorder prediction PloS one Medium 34890409

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Rac1 and Cdc42 capture microtubules through IQGAP1 and CLIP-170. Cell 503 12110184
1999 CLIP-170 highlights growing microtubule ends in vivo. Cell 342 10052454
1992 CLIP-170 links endocytic vesicles to microtubules. Cell 336 1356075
2000 CLIP170-like tip1p spatially organizes microtubular dynamics in fission yeast. Cell 242 11007487
2008 CLIP-170 tracks growing microtubule ends by dynamically recognizing composite EB1/tubulin-binding sites. The Journal of cell biology 239 19103809
1999 Role of dynactin in endocytic traffic: effects of dynamitin overexpression and colocalization with CLIP-170. Molecular biology of the cell 229 10588646
2002 LIS1, CLIP-170's key to the dynein/dynactin pathway. Molecular and cellular biology 208 11940666
2002 Role of dynein, dynactin, and CLIP-170 interactions in LIS1 kinetochore function. The Journal of cell biology 203 11889140
1999 Colocalization of cytoplasmic dynein with dynactin and CLIP-170 at microtubule distal ends. Journal of cell science 178 10212138
2004 Cell cycle control of kinesin-mediated transport of Bik1 (CLIP-170) regulates microtubule stability and dynein activation. Developmental cell 176 15177030
2010 AMPK controls the speed of microtubule polymerization and directional cell migration through CLIP-170 phosphorylation. Nature cell biology 160 20495555
2009 Microtubule plus-end tracking by CLIP-170 requires EB1. Proceedings of the National Academy of Sciences of the United States of America 159 19126680
2016 α-Tubulin Tyrosination and CLIP-170 Phosphorylation Regulate the Initiation of Dynein-Driven Transport in Neurons. Cell reports 155 26972003
2004 Conformational changes in CLIP-170 regulate its binding to microtubules and dynactin localization. The Journal of cell biology 150 15381688
2008 Dynein, Lis1 and CLIP-170 counteract Eg5-dependent centrosome separation during bipolar spindle assembly. The EMBO journal 132 19020519
1998 Evidence for a role of CLIP-170 in the establishment of metaphase chromosome alignment. The Journal of cell biology 130 9585405
2003 Alteration of microtubule dynamic instability during preprophase band formation revealed by yellow fluorescent protein-CLIP170 microtubule plus-end labeling. The Plant cell 109 12615935
1999 Dynamic localization of CLIP-170 to microtubule plus ends is coupled to microtubule assembly. The Journal of cell biology 105 9885247
2005 The microtubule plus-end-tracking protein CLIP-170 associates with the spermatid manchette and is essential for spermatogenesis. Genes & development 101 16230537
1994 Molecular characterization of two functional domains of CLIP-170 in vivo. Journal of cell science 98 7983157
2008 Dynamic behavior of GFP-CLIP-170 reveals fast protein turnover on microtubule plus ends. The Journal of cell biology 95 18283108
2006 Microtubule plus-end loading of p150(Glued) is mediated by EB1 and CLIP-170 but is not required for intracellular membrane traffic in mammalian cells. Journal of cell science 90 16772339
2008 The microtubule-binding protein CLIP-170 coordinates mDia1 and actin reorganization during CR3-mediated phagocytosis. The Journal of cell biology 88 19114595
2002 The FKBP12-rapamycin-associated protein (FRAP) is a CLIP-170 kinase. EMBO reports 86 12231510
2020 ALK rearranged renal cell carcinoma (ALK-RCC): a multi-institutional study of twelve cases with identification of novel partner genes CLIP1, KIF5B and KIAA1217. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 85 32467651
2011 CLIP-170 and IQGAP1 cooperatively regulate dendrite morphology. The Journal of neuroscience : the official journal of the Society for Neuroscience 83 21430156
2010 Phosphorylation of CLIP-170 by Plk1 and CK2 promotes timely formation of kinetochore-microtubule attachments. The EMBO journal 82 20664522
2004 CLIP-170/tubulin-curved oligomers coassemble at microtubule ends and promote rescues. Current biology : CB 82 15589150
2009 CLIP-170-dependent capture of membrane organelles by microtubules initiates minus-end directed transport. Developmental cell 70 19758557
2005 CLIP-170 facilitates the formation of kinetochore-microtubule attachments. The EMBO journal 70 16362039
2008 Lamellar bodies of human epidermis: proteomics characterization by high throughput mass spectrometry and possible involvement of CLIP-170 in their trafficking/secretion. Molecular & cellular proteomics : MCP 68 18622020
2005 Interactions between CLIP-170, tubulin, and microtubules: implications for the mechanism of Clip-170 plus-end tracking behavior. Molecular biology of the cell 68 16120651
1999 Purification and analysis of authentic CLIP-170 and recombinant fragments. The Journal of biological chemistry 62 10464331
2019 Long noncoding RNA ANRIL regulates endothelial cell activities associated with coronary artery disease by up-regulating CLIP1, EZR, and LYVE1 genes. The Journal of biological chemistry 59 30655286
2021 The CLIP1-LTK fusion is an oncogenic driver in non-small-cell lung cancer. Nature 58 34819663
2003 CLIP-170 interacts with dynactin complex and the APC-binding protein EB1 by different mechanisms. Cell motility and the cytoskeleton 54 12789661
2002 CLIPR-59, a new trans-Golgi/TGN cytoplasmic linker protein belonging to the CLIP-170 family. The Journal of cell biology 54 11854307
1999 Alf1p, a CLIP-170 domain-containing protein, is functionally and physically associated with alpha-tubulin. The Journal of cell biology 51 9885248
2006 S. pombe CLASP needs dynein, not EB1 or CLIP170, to induce microtubule instability and slows polymerization rates at cell tips in a dynein-dependent manner. Genes & development 49 16951255
2017 Ninein is essential for apico-basal microtubule formation and CLIP-170 facilitates its redeployment to non-centrosomal microtubule organizing centres. Open biology 47 28179500
2006 CLIP-170 homologue and NUDE play overlapping roles in NUDF localization in Aspergillus nidulans. Molecular biology of the cell 47 16467375
2012 Microtubule-binding protein CLIP-170 is a mediator of paclitaxel sensitivity. The Journal of pathology 46 21989536
2013 Pregnenolone activates CLIP-170 to promote microtubule growth and cell migration. Nature chemical biology 45 23955365
2008 A new role for kinesin-directed transport of Bik1p (CLIP-170) in Saccharomyces cerevisiae. Journal of cell science 45 18411245
2008 The membrane-tubulating potential of amphiphysin 2/BIN1 is dependent on the microtubule-binding cytoplasmic linker protein 170 (CLIP-170). European journal of cell biology 41 19004523
2006 Microtubule binding proteins CLIP-170, EB1, and p150Glued form distinct plus-end complexes. FEBS letters 40 16455083
2011 Interaction of mammalian end binding proteins with CAP-Gly domains of CLIP-170 and p150(glued). Journal of structural biology 36 22119847
2015 Microtubule plus end-associated CLIP-170 initiates HSV-1 retrograde transport in primary human cells. The Journal of cell biology 35 26504169
2002 Microtubule capture: IQGAP and CLIP-170 expand the repertoire. Current biology : CB 35 12361581
2006 The CLIP-170 orthologue Bik1p and positioning the mitotic spindle in yeast. Current topics in developmental biology 33 17118263
2014 CLIP-170 recruits PLK1 to kinetochores during early mitosis for chromosome alignment. Journal of cell science 30 24777477
2014 A defect in the CLIP1 gene (CLIP-170) can cause autosomal recessive intellectual disability. European journal of human genetics : EJHG 29 24569606
2008 Minimal plus-end tracking unit of the cytoplasmic linker protein CLIP-170. The Journal of biological chemistry 28 19074770
2009 Probing interactions between CLIP-170, EB1, and microtubules. Journal of molecular biology 27 19913027
2008 Regulation of lamellipodia formation and cell invasion by CLIP-170 in invasive human breast cancer cells. Biochemical and biophysical research communications 27 18237546
2009 Cdc2-mediated phosphorylation of CLIP-170 is essential for its inhibition of centrosome reduplication. The Journal of biological chemistry 25 19687009
2014 LRRK1-phosphorylated CLIP-170 regulates EGFR trafficking by recruiting p150Glued to microtubule plus ends. Journal of cell science 23 25413345
2017 Cytoplasmic Linker Protein CLIP170 Negatively Regulates TLR4 Signaling by Targeting the TLR Adaptor Protein TIRAP. Journal of immunology (Baltimore, Md. : 1950) 22 29222167
2012 Cooperative stabilization of microtubule dynamics by EB1 and CLIP-170 involves displacement of stably bound P(i) at microtubule ends. Biochemistry 21 22424550
2020 AMPK regulates cell shape of cardiomyocytes by modulating turnover of microtubules through CLIP-170. EMBO reports 20 33251722
1994 Localization of the gene (RSN) coding for restin, a marker for Reed-Sternberg cells in Hodgkin's disease, to human chromosome band 12q24.3 and YAC cloning of the locus. Cytogenetics and cell genetics 20 8222754
2009 Myosin V spatially regulates microtubule dynamics and promotes the ubiquitin-dependent degradation of the fission yeast CLIP-170 homologue, Tip1. Journal of cell science 19 19808886
2002 The cytoplasmic linker protein CLIP-170 is a human autoantigen. Clinical and experimental immunology 19 11966772
2002 Hodgkin and Reed-Sternberg cell-associated autoantigen CLIP-170/restin is a marker for dendritic cells and is involved in the trafficking of macropinosomes to the cytoskeleton, supporting a function-based concept of Hodgkin and Reed-Sternberg cells. Blood 18 12433698
2021 Overexpression of the microtubule-binding protein CLIP-170 induces a +TIP network superstructure consistent with a biomolecular condensate. PloS one 17 34890409
2020 Arsenic trioxide disturbs the LIS1/NDEL1/dynein microtubule dynamic complex by disrupting the CLIP170 zinc finger in head and neck cancer. Toxicology and applied pharmacology 17 32717241
2018 Mapping multivalency in the CLIP-170-EB1 microtubule plus-end complex. The Journal of biological chemistry 17 30455356
2022 Tension of plus-end tracking protein Clip170 confers directionality and aggressiveness during breast cancer migration. Cell death & disease 16 36209218
2021 SOCS3-microtubule interaction via CLIP-170 and CLASP2 is critical for modulation of endothelial inflammation and lung injury. The Journal of biological chemistry 16 33372035
2013 Regulation of tumor angiogenesis by the microtubule-binding protein CLIP-170. Protein & cell 16 23549612
2019 Pregnenolone and pregnenolone-methyl-ether rescue neuronal defects caused by dysfunctional CLIP170 in a neuronal model of CDKL5 Deficiency Disorder. Neuropharmacology 14 31794725
2017 Phosphorylation of EB1 regulates the recruitment of CLIP-170 and p150glued to the plus ends of astral microtubules. Oncotarget 14 28039481
2014 Plk1 phosphorylates CLIP-170 and regulates its binding to microtubules for chromosome alignment. Cell structure and function 14 24451569
2004 CLIP-170 family members: a motor-driven ride to microtubule plus ends. Developmental cell 14 15177023
2018 CLIP-170 is essential for MTOC repositioning during T cell activation by regulating dynein localisation on the cell surface. Scientific reports 13 30487641
2011 Stimulation of the CLIP-170--dependent capture of membrane organelles by microtubules through fine tuning of microtubule assembly dynamics. Molecular biology of the cell 13 21880898
1998 Cloning and expression of chicken CLIP-170 and restin isoforms. Gene 13 9469933
2006 Deletion of RNQ1 gene reveals novel functional relationship between divergently transcribed Bik1p/CLIP-170 and Sfi1p in spindle pole body separation. Current genetics 11 16972090
2020 Stress-induced phosphorylation of CLIP-170 by JNK promotes microtubule rescue. The Journal of cell biology 10 32491151
2017 Adsorption of the natural protein surfactant Rsn-2 onto liquid interfaces. Physical chemistry chemical physics : PCCP 10 28289744
2022 LIS1 interacts with CLIP170 to promote tumor growth and metastasis via the Cdc42 signaling pathway in salivary gland adenoid cystic carcinoma. International journal of oncology 9 36102310
2020 Vibrational spectra, Hirshfeld surface analysis, molecular docking studies of (RS)-N,N-bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide by DFT approach. Heliyon 9 32904270
2016 A role for the yeast CLIP170 ortholog, the plus-end-tracking protein Bik1, and the Rho1 GTPase in Snc1 trafficking. Journal of cell science 9 27466378
1998 Identification and expression of two novel CLIP-170/Restin isoforms expressed predominantly in muscle. Biochimica et biophysica acta 8 9784600
2022 Pregnenolone-methyl-ether enhances CLIP170 and microtubule functions improving spine maturation and hippocampal deficits related to CDKL5 deficiency. Human molecular genetics 7 35348691
2021 Dynactin 1 negatively regulates HIV-1 infection by sequestering the host cofactor CLIP170. Proceedings of the National Academy of Sciences of the United States of America 7 34686593
2019 CLIP-170 spatially modulates receptor tyrosine kinase recycling to coordinate cell migration. Traffic (Copenhagen, Denmark) 7 30537020
2024 Hypothermic oxygenated perfusion inhibits CLIP1-mediated TIRAP ubiquitination via TFPI2 to reduce ischemia‒reperfusion injury of the fatty liver. Experimental & molecular medicine 6 39617791
2022 [A Case of Advanced Lung Squamous Cell Carcinoma with CLIP1-ALK Fusion Gene]. Zhongguo fei ai za zhi = Chinese journal of lung cancer 6 36172736
2015 CLIP-170 tethers kinetochores to microtubule plus ends against poleward force by dynein for stable kinetochore-microtubule attachment. FEBS letters 6 26231764
2024 CLIP170 enhancing FOSL1 expression via attenuating ubiquitin-mediated degradation of β-catenin drives renal cell carcinoma progression. Cellular and molecular life sciences : CMLS 5 39607512
2010 Tip1/CLIP-170 protein is required for correct chromosome poleward movement in fission yeast. PloS one 5 20498706
2022 Rsn-2-mediated directed foam enrichment of β-lactamase. Biotechnology journal 4 35933602
2024 CLIP170 inhibits the metastasis and EMT of papillary thyroid cancer through the TGF-β pathway. Medical oncology (Northwood, London, England) 3 38705933
2019 The concerted actions of Tip1/CLIP-170, Klp5/Kinesin-8, and Alp14/XMAP215 regulate microtubule catastrophe at the cell end. Journal of molecular cell biology 3 31071203
1999 Differential usage of two 5' splice sites in a complex exon generates additional protein sequence complexity in chicken CLIP-170 isoforms. Biochimica et biophysica acta 3 10082970
2022 The CLIP-170 N-terminal domain binds directly to both F-actin and microtubules in a mutually exclusive manner. The Journal of biological chemistry 2 35283190
2012 The cholangiocyte marker, BD. 1, forms a stable complex with CLIP170 and shares an identity with eIF3a, a multifunctional subunit of the eIF3 initiation complex. Experimental and molecular pathology 2 22613460
2024 LTK mutations responsible for resistance to lorlatinib in non-small cell lung cancer harboring CLIP1-LTK fusion. Communications biology 1 38575808
2002 [Expression of p16INK4a, p15INK4b, p21WAF1/Clip1 cell cycle inhibitors on blastic cells in patients with acute myeloblastic leukemia (AML) and acute lymphoblastic leukemia (ALL) ]. Polskie Archiwum Medycyny Wewnetrznej 1 12600181

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