Laurent Bartholin

Transcription activation of FLRG and follistatin by activin A, through Smad proteins, participates in a negative feedback loop to modulate activin A function.

Recurrent involvement of the MLL gene in adult T-lineage acute lymphoblastic leukemia.

Regulation of human erythropoiesis by activin A, BMP2, and BMP4, members of the TGFbeta family.

Drosophila TGIF proteins are transcriptional activators.

FLRG, a new ADAM12-associated protein, modulates osteoclast differentiation.

A novel role for fibronectin type I domain in the regulation of human hematopoietic cell adhesiveness through binding to follistatin domains of FLRG and follistatin.

TGIF inhibits retinoid signaling.

The human Cyr61 gene is a transcriptional target of transforming growth factor beta in cancer cells.

Functional analysis of mutations in TGIF associated with holoprosencephaly.

Identification of NF-kappaB responsive elements in follistatin related gene (FLRG) promoter.

Silencing of FLRG, an antagonist of activin, inhibits human breast tumor cell growth.

AF10-dependent transcription is enhanced by its interaction with FLRG.

Maternal Tgif is required for vascularization of the embryonic placenta.

Generation of mice with conditionally activated transforming growth factor beta signaling through the TbetaRI/ALK5 receptor.

iNKT cell development is orchestrated by different branches of TGF-beta signaling.

Inactivation of TIF1gamma cooperates with Kras to induce cystic tumors of the pancreas.

A rapid strategy to detect the recombined allele in LSL-TβRICA transgenic mice.

Tif1γ suppresses murine pancreatic tumoral transformation by a Smad4-independent pathway.

Premature senescence and increased TGFβ signaling in the absence of Tgif1.

The human NUPR1/P8 gene is transcriptionally activated by transforming growth factor β via the SMAD signalling pathway.

Homotypic cell cannibalism, a cell-death process regulated by the nuclear protein 1, opposes to metastasis in pancreatic cancer.

Generation of a conditional mouse model to target Acvr1b disruption in adult tissues.

The conditional expression of KRAS G12D in mouse pancreas induces disorganization of endocrine islets prior the onset of ductal pre-cancerous lesions.