Recent studies suggest that acetylation of the p53 tumor suppressor protein is not important for its DNA binding activity, as was previously thought. We discuss here a number of theories as to how this modification may serve to regulate the protein’s functions.

The zebrafish is a powerful model system that is poised to contribute to our basic understanding of vertebrate organogenesis. This review develops the theme of modules and illustrates how zebrafish have been particularly useful for understanding heart and blood formation.

This study investigated the role of caspase activation in cardiac contractility and sarcomere organization in the development of CHF.

Here,we summarize the data on which we have built our immunological hypothesis of atherogenesis. This concept is based on the observation that almost all humans have cellular and humoral immune reactions against microbial heat-shock protein 60 (HSP60).

Targeting DNA to mucosal sites through a covalently linked viral adhesin induces strong mucosal cytotoxic T-cell responses. Pathways involving two distinct cell types – dendritic cells and M cells – could mediate DNA sampling at mucosal surfaces.

Working out the draft sequence of the human genome was a landmark achievement. But there’s lots more to be done before the finished product is available. The complete sequence of chromosome 20 sets us on the way.

To take advantage of this, many branches of biology may need to be transformed — moving from bench sciences dominated by competing research groups into collaborative enterprises. This would see entire research communities organized around databases and associated computational tools. In such fields, these online resources could eventually replace the conventional scientific paper as the predominant form of communication.

The p53 protein works to suppress cancer, so one might think that bumping up the levels of this protein would be a good idea. But this isn’t so — mice with too much p53 age prematurely. p53 SIR2

Tumor necrosis factor-α converting enzyme (TACE/ADAM17/CD156q) is a member of the ‘A Disintegrin And Metalloprotease’, or ADAM, family.

To evaluate function, we developed a method for systematic construction of double mutants, termed synthetic genetic array (SGA) analysis, in which a query mutation is crossed to an array of;4700 deletion mutants.

We designed a βA globin gene variant that prevents HbS polymerization and introduced it into a lentiviral vector we optimized for transfer to hematopoietic stem cells and gene expression in the adult red blood cell lineage.

TZD activation of PPAR
may protect against atherosclerosis both by normalizing proatherogenic metabolic abnormalities of the insulin resistance/diabetes milieu and through an inhibition of vascular cell growth and movement.

Experimental research has identified several candidate antigens, and there are encouraging data suggesting that immune modulation as well as immunization can reduce the progression of the disease. This review provides an overview of our current understanding of the role of immune mechanisms in atherosclerosis.

Id proteins (inhibitors of DNA binding/differentiation) are negative regulators of basic helix-loop-helix (bHLH) type transcription factors, which promote the differentiation of various cell types.

Here, we review the mechanisms that lead to this cell cycle and to polyploidy in megakaryocytes, while also comparing them to those described for other systems in which high ploidy is achieved.

The p 63 gene, a member of the p53 gene family, is expressed into at least six protein isoforms which are divided into two groups, those containing the transcription activation domain (TA isoforms) and those that do not (ΔN isoforms).

The most comprehensive Gene Therapy Protocols,including 472 clinical protocols in America and 38 international ones.

Understanding the genetic basis of complex diseases is turning out to be difficult, prompting a widespread (re-)evaluation of the relevant issues.

The elucidation of genetic components of human diseases at the molecular level provides crucial information for developing future causal therapeutic intervention.Here I will discuss the relevance of genome research for disease gene identification and the future progress in molecular medicine.

The study of single nucleotide polymorphisms (SNPs), the most common type of variant, is likely to contribute substantially to deciphering genetic determinants of common and rare diseases.

Here we discuss examples of recent susceptibility studies involving genes, such as those involved in carcinogen metabolism, DNA repair, cell cycle and immune status, that hold the promise of increasing our understanding of cancer etiology and possible prevention strategies.

Development of appropriate tools for assessing clinical phenotypes in mice is a crucial component of these endeavours, as is the establishment of the infrastructure for archiving and distribution of the growing mutant resource to the community.

Comparative sequence analysis of pathogen strains and functional genomics studies are now underway, hopefully providing new insight into infectious disease susceptibility.

Here,we summarize current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, and discuss the potential role of Aβ in this oxidative stress.

DNA fusion vaccines containing immuno-enhancing sequences can augment and direct immune attack on a range of target antigens. Gene-based fusion vaccines offer ease of manipulation and flexible design to activate effective attack on cancer.

In the past two decades, cytogenetic and molecular genetic investigations have revealed that sarcomas are frequently characterized by specific chromosomal translocations, often involving genes encoding transcription factors.

In this review,we present an overview of the field and discuss in depth a few examples of animal models reproducing pathology of human disease with primary and secondary respiratory chain involvement.

Recent studies found evidence of dynamic changes in cellular adhesion and β-catenin localization occurring during invasion, metastasis and expansion of well-differentiated colorectal cancers. It is proposed that such changes might be driven by the local tumor environment, which, if validated,would necessitate a revision of the current linear tumor progression model.

Seeded growth of Aβ1–40 amyloid-like fibrils on a mica surface imaged by atomic force microscopy (AFM).

Survivin is a recently described molecule that has been implicated in both the control of cell proliferation and the regulation of cell lifespan, and is overexpressed in most human cancers.The exploitation of the survivin signaling pathway might provide important predictive and prognostic clues in cancer diagnosis, and offer new therapeutic alternatives for cancer treatment.