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Mouse Anti-EB1 Monoclonal Antibody, Unconjugated, Clone 5

RRID:AB_397892

Antibody ID

AB_397892

Target Antigen

EB1 chicken/avian, human, mouse, rat, chicken, human, mouse, rat

Proper Citation

(BD Biosciences Cat# 610535, RRID:AB_397892)

Clonality

monoclonal antibody

Comments

Immunofluorescence, Immunohistochemistry, Immunoprecipitation, Western blot

Host Organism

mouse

Vendor

BD Biosciences Go To Vendor

Cat Num

610535

Publications that use this research resource

Control of endothelial cell polarity and sprouting angiogenesis by non-centrosomal microtubules.

  • Martin M
  • Elife
  • 2018 Mar 16

Literature context:


Abstract:

Microtubules control different aspects of cell polarization. In cells with a radial microtubule system, a pivotal role in setting up asymmetry is attributed to the relative positioning of the centrosome and the nucleus. Here, we show that centrosome loss had no effect on the ability of endothelial cells to polarize and move in 2D and 3D environments. In contrast, non-centrosomal microtubules stabilized by the microtubule minus-end-binding protein CAMSAP2 were required for directional migration on 2D substrates and for the establishment of polarized cell morphology in soft 3D matrices. CAMSAP2 was also important for persistent endothelial cell sprouting during in vivo zebrafish vessel development. In the absence of CAMSAP2, cell polarization in 3D could be partly rescued by centrosome depletion, indicating that in these conditions the centrosome inhibited cell polarity. We propose that CAMSAP2-protected non-centrosomal microtubules are needed for establishing cell asymmetry by enabling microtubule enrichment in a single-cell protrusion.

Funding information:
  • China Scholarship Council - PhD fellowship()
  • European Research Council - Synergy 609822()
  • Fonds De La Recherche Scientifique - FNRS - FRIA fellowship()
  • H2020 Marie Skłodowska-Curie Actions - IEF fellowship()
  • Marie Sklodowska-Curie Actions - IEF fellowship()
  • NCI NIH HHS - F30 CA183497(United States)
  • Nederlandse Organisatie voor Wetenschappelijk Onderzoek - ALW Open Program grant 824.15.017()

Differentiation between Oppositely Oriented Microtubules Controls Polarized Neuronal Transport.

  • Tas RP
  • Neuron
  • 2017 Dec 20

Literature context:


Abstract:

Microtubules are essential for polarized transport in neurons, but how their organization guides motor proteins to axons or dendrites is unclear. Because different motors recognize distinct microtubule properties, we used optical nanoscopy to examine the relationship between microtubule orientations, stability, and modifications. Nanometric tracking of motors to super-resolve microtubules and determine their polarity revealed that in dendrites, stable and acetylated microtubules are mostly oriented minus-end out, while dynamic and tyrosinated microtubules are oriented oppositely. In addition, microtubules with similar orientations and modifications form bundles that bias transport. Importantly, because the plus-end-directed Kinesin-1 selectively interacts with acetylated microtubules, this organization guides this motor out of dendrites and into axons. In contrast, Kinesin-3 prefers tyrosinated microtubules and can enter both axons and dendrites. This separation of distinct microtubule subsets into oppositely oriented bundles constitutes a key architectural principle of the neuronal microtubule cytoskeleton that enables polarized sorting by different motor proteins.

Funding information:
  • Medical Research Council - G0901533(United Kingdom)

Dynamic Palmitoylation Targets MAP6 to the Axon to Promote Microtubule Stabilization during Neuronal Polarization.

  • Tortosa E
  • Neuron
  • 2017 May 17

Literature context:


Abstract:

Microtubule-associated proteins (MAPs) are main candidates to stabilize neuronal microtubules, playing an important role in establishing axon-dendrite polarity. However, how MAPs are selectively targeted to specific neuronal compartments remains poorly understood. Here, we show specific localization of microtubule-associated protein 6 (MAP6)/stable tubule-only polypeptide (STOP) throughout neuronal maturation and its role in axonal development. In unpolarized neurons, MAP6 is present at the Golgi complex and in secretory vesicles. As neurons mature, MAP6 is translocated to the proximal axon, where it binds and stabilizes microtubules. Further, we demonstrate that dynamic palmitoylation, mediated by the family of α/β Hydrolase domain-containing protein 17 (ABHD17A-C) depalmitoylating enzymes, controls shuttling of MAP6 between membranes and microtubules and is required for MAP6 retention in axons. We propose a model in which MAP6's palmitoylation mediates microtubule stabilization, allows efficient organelle trafficking, and controls axon maturation in vitro and in situ.

Large-Scale Analysis of CRISPR/Cas9 Cell-Cycle Knockouts Reveals the Diversity of p53-Dependent Responses to Cell-Cycle Defects.

  • McKinley KL
  • Dev. Cell
  • 2017 Feb 27

Literature context:


Abstract:

Defining the genes that are essential for cellular proliferation is critical for understanding organismal development and identifying high-value targets for disease therapies. However, the requirements for cell-cycle progression in human cells remain incompletely understood. To elucidate the consequences of acute and chronic elimination of cell-cycle proteins, we generated and characterized inducible CRISPR/Cas9 knockout human cell lines targeting 209 genes involved in diverse cell-cycle processes. We performed single-cell microscopic analyses to systematically establish the effects of the knockouts on subcellular architecture. To define variations in cell-cycle requirements between cultured cell lines, we generated knockouts across cell lines of diverse origins. We demonstrate that p53 modulates the phenotype of specific cell-cycle defects through distinct mechanisms, depending on the defect. This work provides a resource to broadly facilitate robust and long-term depletion of cell-cycle proteins and reveals insights into the requirements for cell-cycle progression.

Funding information:
  • NIGMS NIH HHS - R01 GM088313()
  • NIGMS NIH HHS - R01 GM108718()