Jamal Tazi

Hypermethylation of the cap structure of both yeast snRNAs and snoRNAs requires a conserved methyltransferase that is localized to the nucleolus.

A conserved Drosophila transportin-serine/arginine-rich (SR) protein permits nuclear import of Drosophila SR protein splicing factors and their antagonist repressor splicing factor 1.

mRNA degradation machines in eukaryotic cells.

The RasGAP-associated endoribonuclease G3BP assembles stress granules.

Interaction between the small-nuclear-RNA cap hypermethylase and the spinal muscular atrophy protein, survival of motor neuron.

Sequence-structure-function relationships of Tgs1, the yeast snRNA/snoRNA cap hypermethylase.

Resistance to senescence induction and telomere shortening by a G-quadruplex ligand inhibitor of telomerase.

Altered serine/arginine-rich protein phosphorylation and exonic enhancer-dependent splicing in Mammalian cells lacking topoisomerase I.

Topoisomerase I and II inhibitors control caspase-2 pre-messenger RNA splicing in human cells.

Regulation of cytoplasmic stress granules by apoptosis-inducing factor.

A key role for stress-induced satellite III transcripts in the relocalization of splicing factors into nuclear stress granules.

Selective inhibition of topoisomerase I and various steps of spliceosome assembly by diospyrin derivatives.

The SR protein SC35 is responsible for aberrant splicing of the E1alpha pyruvate dehydrogenase mRNA in a case of mental retardation with lactic acidosis.

Selective modification of alternative splicing by indole derivatives that target serine-arginine-rich protein splicing factors.

The spliceosome: a novel multi-faceted target for therapy.

Control of fetal growth and neonatal survival by the RasGAP-associated endoribonuclease G3BP.

[Selective modification of alternative splicing by indole derivatives that target SR protein splicing factors].

[Alternative splicing: a novel pharmacological target with wide therapeutic potential].

SR proteins as potential targets for therapy.

The SR family proteins B52 and dASF/SF2 modulate development of the Drosophila visual system by regulating specific RNA targets.

Eye development under the control of SRp55/B52-mediated alternative splicing of eyeless.

Inhibition of nonsense-mediated mRNA decay (NMD) by a new chemical molecule reveals the dynamic of NMD factors in P-bodies.

Small-molecule inhibition of HIV pre-mRNA splicing as a novel antiretroviral therapy to overcome drug resistance.

A novel role for PA28gamma-proteasome in nuclear speckle organization and SR protein trafficking.

A large fraction of unclassified variants of the mismatch repair genes MLH1 and MSH2 is associated with splicing defects.

Alternative splicing and disease.

Protection against retrovirus pathogenesis by SR protein inhibitors.

Topoisomerase I suppresses genomic instability by preventing interference between replication and transcription.

Alternative splicing: regulation of HIV-1 multiplication as a target for therapeutic action.

Exon-based clustering of murine breast tumor transcriptomes reveals alternative exons whose expression is associated with metastasis.

Exon definition complexes contain the tri-snRNP and can be directly converted into B-like precatalytic splicing complexes.

The SR protein B52/SRp55 is required for DNA topoisomerase I recruitment to chromatin, mRNA release and transcription shutdown.

Pro-metastatic splicing of Ron proto-oncogene mRNA can be reversed: therapeutic potential of bifunctional oligonucleotides and indole derivatives.

Tissue-specific alternative splicing of Tak1 is conserved in deuterostomes.

A conserved splicing mechanism of the LMNA gene controls premature aging.

Regulated functional alternative splicing in Drosophila.

Splicing-directed therapy in a new mouse model of human accelerated aging.

Revisiting G3BP1 as a RasGAP binding protein: sensitization of tumor cells to chemotherapy by the RasGAP 317-326 sequence does not involve G3BP1.

RBFOX2 is an important regulator of mesenchymal tissue-specific splicing in both normal and cancer tissues.

Deficiency of G3BP1, the stress granules assembly factor, results in abnormal synaptic plasticity and calcium homeostasis in neurons.

Tissue-specific and SRSF1-dependent splicing of fibronectin, a matrix protein that controls host cell invasion.

The sirtuin SIRT6 regulates stress granule formation in C. elegans and mammals.

MBNL1 and RBFOX2 cooperate to establish a splicing programme involved in pluripotent stem cell differentiation.

Antagonistic functions of LMNA isoforms in energy expenditure and lifespan.