doi: 10.1038/embor.2012.48pmid: 22546704
Howy's editorial to accompany the launch of EMBO reports focus series on Sex and Molecular Biology asks whatever happened to the ‘gay gene’.
doi: 10.1038/embor.2012.48pmid: 22546704
Howy's editorial to accompany the launch of EMBO reports focus series on Sex and Molecular Biology asks whatever happened to the ‘gay gene’.
doi: 10.1038/embor.2012.45pmid: 22546705
The ‘sex and science’ focus series in EMBO reports will highlight the biological and social importance of sex, and the contribution of science to understanding its influence.
doi: 10.1038/embor.2012.43pmid: 22473296
Scientists in developing countries face lower absolute levels of funding and often have to pay scandalously higher prices for consumables and equipment.
doi: 10.1038/embor.2012.47pmid: 22491027
Could it be that stemness is not a specific fate resulting from a distinct stem‐cell programme, but simply a result of a stem cell escaping ulterior differentiation? Stemness could be entirely intrinsic to non‐differentiated cells.
doi: 10.1038/embor.2012.50pmid: 22491033
Declining sperm counts and the increasing average age of first‐time parents spell trouble for human fertility, especially when set against the backdrop of ageing populations.
Vasconcelos, Sonia M R; Steneck, Nicholas H; Anderson, Melissa; Masuda, Hatisaburo; Palacios, Marisa; Pinto, José C S; Sorenson, Martha M
doi: 10.1038/embor.2012.51pmid: 22491030
The science ethics melting pot is just heating up; what role will emerging nations play in setting new standards of practice that ensure successful international collaborations?
doi: 10.1038/embor.2012.49pmid: 22491028
Despite not yet living up to the early hype, systems biology has become an integral component of biological research and should soon yield its first tangible results.
doi: 10.1038/embor.2012.41pmid: 22473297
Several bone marrow‐derived cells have been shown to promote tumour growth and progression. These cells can home to the primary tumour and become active components of the tumour microenvironment. Recent studies have also identified bone marrow‐derived cells—such as mesenchymal stem cells and regulatory T cells—as contributors to cancer metastasis. The innate versatility of these cells provides diverse functional aid to promote malignancy, ranging from structural support to signal‐mediated suppression of the host immune response. Here, we review the role of mesenchymal stem cells and regulatory T cells in cancer metastasis. A better understanding of the bipolar nature of these bone marrow‐derived cells in physiological and malignant contexts could pave the way for new therapeutics against metastatic disease.
Ong, Chin‐Tong; Corces, Victor G
doi: 10.1038/embor.2012.52pmid: 22491032
Enhancers are regulatory DNA elements that dictate the spatial and temporal patterns of gene expression during development. Recent evidence suggests that the distinct chromatin features of enhancer regions provide the permissive landscape required for the differential access of diverse signalling molecules that drive cell‐specific gene expression programmes. The epigenetic patterning of enhancers occurs before cell fate decisions, suggesting that the epigenetic information required for subsequent differentiation processes is embedded within the enhancer element. Lineage studies indicate that the patterning of enhancers might be regulated by the intricate interplay between DNA methylation status, the binding of specific transcription factors to enhancers and existing histone modifications. In this review, we present insights into the mechanisms of enhancer function, which might ultimately facilitate cell reprogramming strategies for use in regenerative medicine.
Garcia, Julie; Sandi, Maria José; Cordelier, Pierre; Binétruy, Bernard; Pouysségur, Jacques; Iovanna, Juan Lucio; Tournaire, Roselyne
doi: 10.1038/embor.2012.29pmid: 22421998
Endothelial–mesenchymal transition (EndMT) has a significant role in embryonic heart formation and in various pathologies. However, the molecular mechanisms that regulate EndMT induction remain to be elucidated. We show that suppression of receptor tyrosine kinase Tie1 but not Tie2 induces human endothelial cells to undergo EndMT and that Slug deficiency reverts this process. We find that Erk1/2, Erk5 and Akt cascades control Slug promoter activity induced by Tie1 deficiency. Interestingly, EndMT is present in human pancreatic tumour. We propose that EndMT associated with Tie1 downregulation participates in the pathological development of stroma observed in tumours.
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