Presentation is loading. Please wait.

Presentation is loading. Please wait.

Colocalization of the human trimethylguanosine synthase 1 and survival of motor neuron proteins. Colocalization of the human trimethylguanosine synthase.

Published byHartono Halim Modified over 5 years ago

Similar presentations

Presentation on theme: "Colocalization of the human trimethylguanosine synthase 1 and survival of motor neuron proteins. Colocalization of the human trimethylguanosine synthase."— Presentation transcript:

1 Colocalization of the human trimethylguanosine synthase 1 and survival of motor neuron proteins.
Colocalization of the human trimethylguanosine synthase 1 and survival of motor neuron proteins. HeLa cells carrying green fluorescent protein (GFP)–trimethylguanosine‐synthase‐1 (TGS1; upper row), GFP–survival‐of‐motor‐neuron (SMN; middle row) or GFP–SMNΔN27 (lower row) constructs were examined by immunofluorescence microscopy using anti‐SMN or anti‐TGS1 antibodies. Colocalization of the GFP fusion proteins (green) and SMN or TGS1 (red) is indicated by the yellow colour in the combined panels. DNA was stained with 4,6‐diamidino‐2‐phenylindole (DAPI; blue). John Mouaikel et al. EMBO Rep. 2003;4: © as stated in the article, figure or figure legend

Download ppt "Colocalization of the human trimethylguanosine synthase 1 and survival of motor neuron proteins. Colocalization of the human trimethylguanosine synthase."

Similar presentations

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.
Survivin is a determining factor for mitotic localization of the chromosome passenger complex. Survivin is a determining factor for mitotic localization.

Survivin is a determining factor for mitotic localization of the chromosome passenger complex. Survivin is a determining factor for mitotic localization.
Prolyl‐hydroxylase‐domain proteins regulate hypoxia inducible factor‐α in response to O2 availability. Prolyl‐hydroxylase‐domain proteins regulate hypoxia.

Prolyl‐hydroxylase‐domain proteins regulate hypoxia inducible factor‐α in response to O2 availability. Prolyl‐hydroxylase‐domain proteins regulate hypoxia.
E2F7/8 and HIF1 are required for hypoxic VEGFA expression.

E2F7/8 and HIF1 are required for hypoxic VEGFA expression.
Defective phenotypes of ts alp4 and alp6 mutants and the cellular localization of Alp4 and Alp6 at the MTOC. (A) Wild‐type (left, HM123, Table II), alp4‐1891.

Defective phenotypes of ts alp4 and alp6 mutants and the cellular localization of Alp4 and Alp6 at the MTOC. (A) Wild‐type (left, HM123, Table II), alp4‐1891.
Co‐localization of recombination proteins with double‐strand breaks.

Co‐localization of recombination proteins with double‐strand breaks.
Statistical analysis of transgene expression in pigs generated by lentiviral gene transfer. Statistical analysis of transgene expression in pigs generated.

Statistical analysis of transgene expression in pigs generated by lentiviral gene transfer. Statistical analysis of transgene expression in pigs generated.
DNA‐anchored LacI–CFP–Luciferase aggregates capture misfolded cytosolic proteins. DNA‐anchored LacI–CFP–Luciferase aggregates capture misfolded cytosolic.

DNA‐anchored LacI–CFP–Luciferase aggregates capture misfolded cytosolic proteins. DNA‐anchored LacI–CFP–Luciferase aggregates capture misfolded cytosolic.
REF and ATP5b status on mitochondrial fraction.

REF and ATP5b status on mitochondrial fraction.
Internalization of kinase‐dead epidermal growth factor receptor K721A

Internalization of kinase‐dead epidermal growth factor receptor K721A
Yeast Tgl3p expressed in HeLa cells localizes to lipid droplets.

Yeast Tgl3p expressed in HeLa cells localizes to lipid droplets.
Periodic changes in distribution of ERK–GFP fusion protein in cells after stimulation with EGF. (A) Confocal image of cells expressing ERK–GFP both before.

Periodic changes in distribution of ERK–GFP fusion protein in cells after stimulation with EGF. (A) Confocal image of cells expressing ERK–GFP both before.
SERCA2 is a functional adaptor for the alternative toll‐like receptor 9 (TLR9) signalling in cardiomyocytes Co‐immunoprecipitated TLR9 with SERCA2 antibody.

SERCA2 is a functional adaptor for the alternative toll‐like receptor 9 (TLR9) signalling in cardiomyocytes Co‐immunoprecipitated TLR9 with SERCA2 antibody.
The absence of Yca1 attenuates the apoptotic phenotypes of lsm4 mutants. The absence of Yca1 attenuates the apoptotic phenotypes of lsm4 mutants. (A) Wild‐type.

The absence of Yca1 attenuates the apoptotic phenotypes of lsm4 mutants. The absence of Yca1 attenuates the apoptotic phenotypes of lsm4 mutants. (A) Wild‐type.
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.
Dynamics of ookinete to oocyst transition, and effects of SRPN2 knockdown. Dynamics of ookinete to oocyst transition, and effects of SRPN2 knockdown. Mosquitoes.

Dynamics of ookinete to oocyst transition, and effects of SRPN2 knockdown. Dynamics of ookinete to oocyst transition, and effects of SRPN2 knockdown. Mosquitoes.
Induction of apoptosis by CDIP expression.

Induction of apoptosis by CDIP expression.
Set9 inhibits oxidative stress‐induced neuronal cell death via methylation of FOXO3. Set9 inhibits oxidative stress‐induced neuronal cell death via methylation.

Set9 inhibits oxidative stress‐induced neuronal cell death via methylation of FOXO3. Set9 inhibits oxidative stress‐induced neuronal cell death via methylation.
Induction of DNA double‐strand breaks and activation of the ataxia telangiectasia mutated pathway in post‐mitotic cells in response to camptothecin. Induction.

Induction of DNA double‐strand breaks and activation of the ataxia telangiectasia mutated pathway in post‐mitotic cells in response to camptothecin. Induction.
Relocalisation of both MK5 and ERK3 requires a CRM1‐dependent nuclear export pathway. Relocalisation of both MK5 and ERK3 requires a CRM1‐dependent nuclear.

Relocalisation of both MK5 and ERK3 requires a CRM1‐dependent nuclear export pathway. Relocalisation of both MK5 and ERK3 requires a CRM1‐dependent nuclear.

Similar presentations

Ads by Google