S.A. Brown

Discipline

Type de document

Articles (6) Recensions (1)

Co-auteur

A. Kramer

M. Sato

A. Liechti

G. Katsioudi

D. Gatfield

S. Gaspari

C.H. Gabriel

R. Dreos

E.S. Arpa

T.S. Zheng

H. Yagita

P.Y. Wu

J.A. Winkles

S. Weng

M. Wang

M. Vaas

S.K. Tyagarajan

Z.S. Thirouin

TJJ Sudharshan

R. Shi

M.L. Scott

P. Schneider

S. Sampath

K. Popadin

R.C. Paolicelli

P. Panzanelli

S.B. Noya

E. Moriggi

J.B. Miller

J.S. Michaelson

R.A. McKinney

D. Mauvoisin

F. Martineau

B. Maier

D. Kunz

C.A. Kostek

J. Klohs

Y.M. Hsu

C. Howald

M. Gutierrez-Arcelus

M. Girgenrath

R. Gill

L. Gaspar

F. Gachon

R.A. Flavell

E. Falconnet

E.T. Dermitzakis

T. Cramer

D. Colameo

P.K. Chang

L.C. Burkly

B. Browning

C. Borel

P.A. Barker

S.E. Antonarakis

N. Allaire

Date

Source

Serveur académique Lausannois (5) Acta Theologica (1)

Mot-clé

Stability (4) Mice (4) Gene expression (4) Stability (4) protéine (3) physiologie (3) Physiology (3) RNA (3) Physiology (3) Human beings (3) Liver (3) Animals (3) roman (3) surveillance (2) traitement (2) mutant (2) modèle (2) gène (2) règlement (2) Decay (2) Transcription (2) Messenger RNA (2) Functions (2) Expression (2) Example (2) Errors (2) Cytology (2) Regulation (2) Receptors (2) Transcription (2)

Documents écrit par S.A. Brown (6) | parle de S.A. Brown (1)

A conditional Smg6 mutant mouse model reveals circadian clock regulation through the nonsense-mediated mRNA decay pathway.

G. Katsioudi et al. (13 janv. 2023)

A novel Smg6 mouse model reveals regulation of circadian period and daily CRY2 accumulation through the nonsense-mediated mRNA decay pathway

G. Katsioudi et al. (3 juil. 2022)

Cross-talk between GABAergic postsynapse and microglia regulate synapse loss after brain ischemia.

T. Cramer et al. (4 mars 2022)

Preaching when viral threats converge: USA sermons, 31 May and 7 June 2020

S.A. Brown (1 janv. 2020)

The genomic landscape of human cellular circadian variation points to a novel role for the signalosome.

L. Gaspar et al. (4 sept. 2017)

TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration.

M. Girgenrath et al. (2006)