Presentation is loading. Please wait.

Presentation is loading. Please wait.

The WD domain of ATG16L1 is not required for canonical autophagy

Published byDouglas Marsh Modified over 6 years ago

Similar presentations

Presentation on theme: "The WD domain of ATG16L1 is not required for canonical autophagy"— Presentation transcript:

1 The WD domain of ATG16L1 is not required for canonical autophagy
The WD domain of ATG16L1 is not required for canonical autophagy ADiagram of full‐length (FL) 229–242 deletion (ΔFBD) and 1–336 (ΔWD) ATG16L1 constructs used in this study.B‐DWestern blot analysis of ATG16L1 in (B) HCT116 ATG16L1−/−, (C) MEF Atg16L1−/− and (D) MCF10A ATG16L1−/− cells stably re‐expressing ATG16L1 constructs. Arrows indicate specific ATG16L1 band.EWestern blotting for LC3 in complemented HCT116 cells ± PP242 (1 μM, 1 h).FQuantification of fold differences of LC3‐II/LC3‐I ratios over controls from (E).GConfocal images of GFP‐LC3 in complemented MEF cells ± starvation (1 h). Scale bar: 10 μm.HQuantification of GFP‐LC3 puncta from 100 MEF cells per experiment cultured in full media (control) or EBSS (starve) for 1 h.IQuantification of WIPI2b puncta in ATG16L1‐complemented HCT116 cells. Puncta from 100 cells were counted per experiment.Data information: Data represent mean ± SEM from three separate experiments. (F) *P < 0.02. (H) ***P < 0.0001, **P <  (I) ***P < 0.0006, **P≪0.005 (Student's t‐test). Katherine Fletcher et al. EMBO J. 2018;embj © as stated in the article, figure or figure legend

Download ppt "The WD domain of ATG16L1 is not required for canonical autophagy"

Similar presentations

The basal and stress‐induced activity of HSF1 is impaired in human aneuploid cells A, BWestern blot analysis for HSP27, HSP70, HSP90 (the used antibody.

The basal and stress‐induced activity of HSF1 is impaired in human aneuploid cells A, BWestern blot analysis for HSP27, HSP70, HSP90 (the used antibody.
Effects of inhibiting inflammatory cell recruitment on fracture healing Treatment with CCR2 antagonist, INCB3344, led to impaired fracture healing compared.

Effects of inhibiting inflammatory cell recruitment on fracture healing Treatment with CCR2 antagonist, INCB3344, led to impaired fracture healing compared.
Validating Cdk‐dependent chromatin association changes of selected outliers A–EValidation of changes in chromatin affinity following Cdk inhibition of.

Validating Cdk‐dependent chromatin association changes of selected outliers A–EValidation of changes in chromatin affinity following Cdk inhibition of.
Overexpression of PAI‐1 reverses the arsenite‐mediated effect on senescence Overexpression of PAI‐1 reverses the arsenite‐mediated effect on senescence.

Overexpression of PAI‐1 reverses the arsenite‐mediated effect on senescence Overexpression of PAI‐1 reverses the arsenite‐mediated effect on senescence.
Reduction in immune cell infiltration after stab wound injury in CCR2−/− mice increases proliferation at the injury site Reduction in immune cell infiltration.

Reduction in immune cell infiltration after stab wound injury in CCR2−/− mice increases proliferation at the injury site Reduction in immune cell infiltration.
Morphology of white adipose tissue and muscle in S1/3 KO mice of different ages Morphology of white adipose tissue and muscle in S1/3 KO mice of different.

Morphology of white adipose tissue and muscle in S1/3 KO mice of different ages Morphology of white adipose tissue and muscle in S1/3 KO mice of different.
Juxtavascular astrocytes are enriched in nuclear Aryl hydrocarbon receptor immunostaining at the stab wound injury site in WT mice Juxtavascular astrocytes.

Juxtavascular astrocytes are enriched in nuclear Aryl hydrocarbon receptor immunostaining at the stab wound injury site in WT mice Juxtavascular astrocytes.
Reduced astrocyte proliferation results in increased immune cell infiltration into the injured GM Reduced astrocyte proliferation results in increased.

Reduced astrocyte proliferation results in increased immune cell infiltration into the injured GM Reduced astrocyte proliferation results in increased.
Reduced scar formation in the injured GM of CCR2−/− mice

Reduced scar formation in the injured GM of CCR2−/− mice
Surface distribution of immunogold‐labelled PS I (A–C) and ATP synthase (D–F) complexes. Surface distribution of immunogold‐labelled PS I (A–C) and ATP.

Surface distribution of immunogold‐labelled PS I (A–C) and ATP synthase (D–F) complexes. Surface distribution of immunogold‐labelled PS I (A–C) and ATP.
Resveratrol inhibits the transactivation potential of the RelA/p65 protein. Resveratrol inhibits the transactivation potential of the RelA/p65 protein.

Resveratrol inhibits the transactivation potential of the RelA/p65 protein. Resveratrol inhibits the transactivation potential of the RelA/p65 protein.
Loss of USP8 or HIF1α impairs endocytic recycling required for ciliogenesis Kinetic analysis of transferrin recycling measured by flow cytometry. Loss.

Loss of USP8 or HIF1α impairs endocytic recycling required for ciliogenesis Kinetic analysis of transferrin recycling measured by flow cytometry. Loss.
Rab22A regulates melanocyte pigmentation, cargo transport and functions upstream of BLOC‐1 Rab22A regulates melanocyte pigmentation, cargo transport and.

Rab22A regulates melanocyte pigmentation, cargo transport and functions upstream of BLOC‐1 Rab22A regulates melanocyte pigmentation, cargo transport and.
HDAC3 regulates AKT phosphorylation

HDAC3 regulates AKT phosphorylation
AO domain of LSD1 is responsible for its interaction with Snail1.

AO domain of LSD1 is responsible for its interaction with Snail1.
Optical labelling by two‐photon excitation.

Optical labelling by two‐photon excitation.
Mitophagy is independent of PINK1 and Parkin.

Mitophagy is independent of PINK1 and Parkin.
The HDAC3 inhibitor suppresses SPOP‐mutated prostate cancer cell growth The HDAC3 inhibitor suppresses SPOP‐mutated prostate cancer cell growth A22Rv1.

The HDAC3 inhibitor suppresses SPOP‐mutated prostate cancer cell growth The HDAC3 inhibitor suppresses SPOP‐mutated prostate cancer cell growth A22Rv1.
Subcellular localization of full‐length and cleaved PINK1 PINK1 immunoblot of cytoplasmic and mitochondrial fractions from HeLa cells transfected with.

Subcellular localization of full‐length and cleaved PINK1 PINK1 immunoblot of cytoplasmic and mitochondrial fractions from HeLa cells transfected with.
Neuro‐inflammatory cytokines, brain microglial activation, and working memory deficits are normalized using LV.IDS.ApoEII, but not LV.IDS in MPS II mice.

Neuro‐inflammatory cytokines, brain microglial activation, and working memory deficits are normalized using LV.IDS.ApoEII, but not LV.IDS in MPS II mice.

Similar presentations

Ads by Google