Fig. 4. Co-immunostaining of nocodazole or ASNase treated RPE-1 cells with anti-hASNS and anti-alpha tubulin showed defect in both mitotic spindle formation.

Slides:

Advertisements

Similar presentations

Fig. 5. Prip silencing enhances the co-localization of GABARAP with insulin vesicles and β-tubulin.Co-localization of GABARAP (green) with insulin (red)

Advertisements

Fig. 1. Overview of the nervous system of the adult S. roscoffensis.

Fig. 2. Outline of the two types of stimulus sequences employed in the analysis.(A) Environment information stimuli; (B) adaptation stimuli. Outline of.

Fig. 8. CCA and ChQ treatment induce accumulation of F-actin rings.

Fig. 1. Representative images of the four cell lines using fluorescence microscopy. Representative images of the four cell lines using fluorescence microscopy.

Fig. 4. E-cadherin expression level affects monomer dynamics.

Fig. 5. Effect of MPO on surface elasticity of human platelets

Fig. 2. Morphological changes of cultured adherent fibroblastic cells after OA treatment related to actin microfilament reorganization.(A) Cells observed.

Nephrogenesis in vitro can be rescued in 3D co-cultures by siRNA treatment of Renca cells. Nephrogenesis in vitro can be rescued in 3D co-cultures by siRNA.

Fig. 7. Motion adaptation increases time-dependent response modulations (TDRM) relatively to the average cell response.TDRM normalized to the value obtained.

Fig. 2. Proportion of motile objects and track length

Fig. 3. Knockdown of cited3 results in increased cell death but it does not affect proliferation.Embryos that are injected with the control MO (A–C), cited3.

TC-1 silencing sensitized A549 and SPC-A-1 cells to radiation therapy

Fig. 6. Comparison between the response against transformed tissues and capsule formation.At the cellular level the two responses share many similarities.

Fig. 2. Histone H3 phosphorylation appears at prometaphase upon C4 treatment.(A) Western blots were realized on cells synchronized at mitotic entry in.

Fig. 7. Knockdown of Meis1 abolishes CR4. 2-GFP expression

Fig. 1. Mitochondrial internalization in cardiomyocytes.

Fig. 3. Read-outs of mTORC1 (P-S6(S235/236)) and mTORC2 (P-Akt(S473)) in wtPC12 and PC12-27 cells.(A,B) wtPC12 and PC12-27 cells were treated for 48 hr.

Fig. 3. Inactivation of the Wnt/β-catenin signaling pathway inhibited cell proliferation and induced apoptosis in A549 and SPC-A-1 cells. Inactivation.

Fig. 1. Loss of PC following INT depletion

Fig. 1. Lack of Hmga1 and Hmga2 expression in A1/A2-KO mice

Fig. 1. Morphological and growth characterization of hBMCs and hPDCs

Fig. 4. The model of malate metabolism in fruit cells under different K level conditions. The model of malate metabolism in fruit cells under different.

Fig. 4. Acentriolar mitotic spindle assembly

Fig. 5. Recovery steps of mitotic acentriolar cells after cold MT depolymerisation.(A,B) Time-lapse sequences of mitotic spindle re-formation at 18°C.

Fig. 1. Pigmentation and melanophore counts of rainbow trout parr and smolt caudal fins.Pigmentation of (A) parr and (B) smolt. Pigmentation and melanophore.

Fig. 3. Relative expression levels of ASNS to α-tubulin were dramatically increased when treating human cells with nocodazole and ASNase. Relative expression.

Fig. 6. LR phenotype of plastid translation-defective mutants with/without Spec. LR phenotype of plastid translation-defective mutants with/without Spec.

Fig. 1. Co-immunostaining of yeast spheroplasts with anti-hASNS and anti-alpha tubulin revealed that yeast asparagine synthetases formed filaments/foci.

Wound recruitment of melanocytes requires innate immune cells.

Fig. 3. The checkpoint proteins Mad2 and BubR1 remain associated with the kinetochores of unaligned chromosomes in cenp-metaΔ mutant cells entering anaphase.(A–C)

Fig. 8. C. elegans susceptibility to α-terthienyl was affected by the activities of skn-1 and wdr-23. C. elegans susceptibility to α-terthienyl was affected.

Fig. 5. GFP fluorescence colocalization of Gcn5.

Fig. 2. Morphological analysis of acentriolar mitotic spindles

Fig. 5. Receptor tyrosine kinase activation in response to growth factor stimulation. Receptor tyrosine kinase activation in response to growth factor.

The TER94-p47 complex isinvolved in Notch signaling regulation

Fig. 3. Rnd proteins induce stronger responses in subconfluent endothelial cells.HUVECs were transfected with Rnd1, Rnd2, Rnd3 or GFP-encoding plasmids.

Fig. 2. Soluble sugar and organic acid levels with different K fertilization during fruit development. Soluble sugar and organic acid levels with different.

Fig. 4. BKA values for different species.

Fig. 7. Representative images of control (Cas9+GFP) and Cas9+gRNA+GFP co-injected embryos on day 4 of culture, showing nuclear-imported GFP (green) and.

Fig. 7. Ror-GFP binds to Myc-tagged Wnts and Wnt receptors.

Fig. 1. Mitotic arrest results in differential RNA association with coilin.Untreated or nocodazole treated HeLa cell lysate was used for RNA immunoprecipitations.

Statistical chart of significantly differentially expressed genes

Fig. 3. Analysis of mitotic and post-mitotic specificity of recombination in the cerebral cortices of Emx1cre and Nestin-cre mice using the MADM-11 genetic.

Fig. 6. Meis1 protein is present in CR4. 2-GFP+ and Foxn4+ cells

Fig. 9. Mip120 CXC and HCH domains are not sufficient for nuclear localization in mip120 null egg chambers. Mip120 CXC and HCH domains are not sufficient.

Fig. 1. Phenotypic characterisation of primary human tubular epithelial cells and human renal fibroblasts. Phenotypic characterisation of primary human.

Fig. 4. Perinuclear dynein regulators are not required for primary ciliogenesis.RPE cells were transfected with siRNA and either nocodazole-treated, fixed,

Fig. 1. Loss of PC following INT depletion

Fig. 8. Tracking details and coordinate systems.

Fig. 2. iPSCs produce functional osteoblasts.

Fig. 12. Overview of the molecular program essential to build mdDA neurons.The genes identified in this study (in red) have been added to the programming.

Fig. 2. Coupling of actin to cell–cell junctions requires α-catenin and is necessary for the establishment of the barrier.(A) Effect of Cytochalasin D.

Morphological changes induced by T3 treatment in trβ crispants

Fig. 3. transparent is required cell-autonomously in iridophores

Fig. 4. CR4.2 may be active in amacrine cells but not in ganglion cells.Chick retinas were electroporated with either the control CAG-GFP construct or.

Fig. 2. Acetylation stiffens primary cilia.

EB1 and its C-terminal binding partner APC co-purify with centrosomes.

Depletion of EB1 with small interfering RNA reduces MT minus-end anchoring at the centrosome. Depletion of EB1 with small interfering RNA reduces MT minus-end.

Fig. 6. RhoB is required for Rnd3-induced stress fibre formation

Fig. 7. Eye defects in STK35 KO mouse.

Fig. 3. Mean force and velocity during jumping

mip120 null egg chambers have a condensed nurse cell DNA phenotype

Fig. 6. Bj mutants show stereocilia patterning defects and biliary duct (BD) malformations. Bj mutants show stereocilia patterning defects and biliary.

Table 1. Measurement of ring diameters of proteins localizing in ring-like patterns around centrioles.Consideration of the size of IgG (about 8 nm) raises.

Fig. 5. Behaviours of the wild-types Oregon-R at two temperatures.

WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates TfR. WT MARCH8, but not the CS mutant, specifically ubiquitinates and downregulates.

Maytansinol disrupts the mitotic spindle and prevents mitotic exit in Drosophila. Maytansinol disrupts the mitotic spindle and prevents mitotic exit inDrosophila.

Disruption of the tubule formation by immortalized cells during nephrogenesis in vitro. Disruption of the tubule formation by immortalized cells during.

Phenotype of S. pombe cells in the presence of B21P2 or LMB

Presentation transcript:

Fig. 4. Co-immunostaining of nocodazole or ASNase treated RPE-1 cells with anti-hASNS and anti-alpha tubulin showed defect in both mitotic spindle formation of tubulins and spindle-like patterning of ASNS. (A) RPE-1 cells were first grown for 2 days, treated with either 100 ng/ml nocodazole for 16 h (A) or 2 U/ml ASNase for 2 days (B), then fixed with paraformaldehyde, and immunostained with anti-hASNS (red) and anti-alpha tubulin (green). Co-immunostaining of nocodazole or ASNase treated RPE-1 cells with anti-hASNS and anti-alpha tubulin showed defect in both mitotic spindle formation of tubulins and spindle-like patterning of ASNS. (A) RPE-1 cells were first grown for 2 days, treated with either 100 ng/ml nocodazole for 16 h (A) or 2 U/ml ASNase for 2 days (B), then fixed with paraformaldehyde, and immunostained with anti-hASNS (red) and anti-alpha tubulin (green). Chalongrat Noree et al. Biology Open 2018;7:bio038307 © 2018. Published by The Company of Biologists Ltd