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RNAEDIT

Financiado

Cerrado

RNA EDITING IN HEALTH AND DISEASE

"RNA editing is a type of programmed RNA sequence alteration that can result in a range of proteomic changes, from subtle fluctuations in output, to specific alterations in protein content. Editing is catalyzed by two classes of d... ver más

31/12/2021

GERMAN CANCER RESE...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Ver 3 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-12-31

ERC-CoG-2014: ERC Consolidator Grant

I+D

Cerrada hace 10 años

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No hay información privada compartida para este proyecto. Habla con el coordinador.

3 Participantes

GERMAN CANCER RESEARCH CENTE...

1.84M€ | Lider

430.83K€ | Participante

THE CHANCELLOR MASTERS AND S...

N.D. | Participante

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Duración del proyecto: 74 meses Fecha Inicio: 2015-10-01
Fecha Fin: 2021-12-31

Líder del proyecto

DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto "RNA editing is a type of programmed RNA sequence alteration that can result in a range of proteomic changes, from subtle fluctuations in output, to specific alterations in protein content. Editing is catalyzed by two classes of deaminases: those which convert adenosine to inosine (ADARs) and those which convert cytosine to uracil (APOBEC1). We have previously shown that APOBEC1-catalyzed editing in the transcriptome of macrophages leads to the generation of populations that are heterogeneous, and functionally diverse, enabling rapid population adaptation to different environmental settings. Our first aim for this proposal is to extend our studies to additional immune cell subsets, focusing on cells that are recently recognized as ""plastic"" to define the contribution of editing to this plasticity of fate and function. RNA editing of the type we study has also been demonstrated to be crucial for cancer progression. For instance, APOBEC1-deficiency significantly reduces tumour burden on cells of the intestine and colon that are prone to adenocarcinomas in the context of the APC-min mutation. This is also the case for testicular carcinomas in mouse models of such tumours. Thus, there is genetic evidence for a requirement for APOBEC1 and RNA editing to drive tumour progression, in two tumour contexts. Based on these data and on our recently deciphered role for APOBEC1 as a ""stealthy"" diversifier of cellular transcriptomes (and proteomic outcomes), we hypothesize that APOBEC1 drives tumour progression by editing select transcripts in tumour cells (or tumour stem cells), thus enabling the rapid adaptation of the tumour to the onslaught of the immune response. Our second aim is to characterize the subset of edited transcripts in these model tumours (either at the population or at the single cell level) and understand their role to tumour survival and progression, both in mouse models of disease, and in human tumour samples (in collaboration with QP Hammarstrom, KI)."

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