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Human Molecular Genetics
The journal concentrates on full-length research papers covering a wide range of topics in all aspects of human molecular genetics, including the molecular basis of human genetic disease; developmental genetics; cancer genetics; neurogenetics; chromosome and genome structure and function; gene therapy; mouse and other models of human diseases; functional genomics; and computational genomics.
Flk1-positive cells derived from embryonic stem cells serve as vascular progenitors
It is shown that Flk1+ cells derived from embryonic stem cells can differentiate into both endothelial and mural cells and can reproduce the vascular organization process and offer potential for tissue engineering of the vascular system.
p140mDia, a mammalian homolog of Drosophila diaphanous,is a target protein for Rho small GTPase and is a ligand for profilin
Results suggest that Rho regulates actin polymerization by targeting profilin via p140mDia beneath the specific plasma membranes.
Ptf1a, a bHLH Transcriptional Gene, Defines GABAergic Neuronal Fates in Cerebellum
ROCK‐I and ROCK‐II, two isoforms of Rho‐associated coiled‐coil forming protein serine/threonine kinase in mice
Nonadipose tissue production of leptin: Leptin as a novel placenta-derived hormone in humans
Evidence is provided for leptin as a novel placenta-derived hormone in humans and the physiologic and pathophysiologic significance of leptin in normal pregnancy and gestational trophoblastic neoplasms is suggested.
Differentiation of embryonic stem cells is induced by GATA factors.
It is reported that forced expression of either Gata-6 or Gata -4 in embryonic stem (ES) cells is sufficient to induce the proper differentiation program towards ExE, the first report of a physiological differentiation event induced by the ectopic expression of a transcription factor in ES cells.
Role of premature leptin surge in obesity resulting from intrauterine undernutrition.
A missense mutation of the endothelin-B receptor gene in multigenic hirschsprung's disease
Thyroid hormone action is disrupted by bisphenol A as an antagonist.
- K. Moriyama, T. Tagami, K. Nakao
- Biology, MedicineJournal of Clinical Endocrinology and Metabolism
- 1 November 2002
The results suggest that BPA could displace T(3) from the TR and recruit a transcriptional repressor, resulting in gene suppression, the first report that B PA can antagonize T( 3) action at the transcriptional level.