Presentation is loading. Please wait.

Presentation is loading. Please wait.

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.

Published byÈve Lepage Modified over 5 years ago

Similar presentations

Presentation on theme: "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."— Presentation transcript:

1 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 © Published by The Company of Biologists Ltd

Download ppt "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."

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)

Fig. 5. Prip silencing enhances the co-localization of GABARAP with insulin vesicles and β-tubulin.Co-localization of GABARAP (green) with insulin (red)
Fig. 1. Overview of the nervous system of the adult S. roscoffensis.

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. 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. 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. 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. 4. E-cadherin expression level affects monomer dynamics.
Fig. 5. Effect of MPO on surface elasticity of human platelets

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.

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.

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. 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. 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.

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

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. 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. 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. 7. Knockdown of Meis1 abolishes CR4. 2-GFP expression
Fig. 1. Mitochondrial internalization in cardiomyocytes.

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. 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. 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. Loss of PC following INT depletion

Similar presentations

Ads by Google