Anomalous Creation of Branes

In certain circumstances when two branes pass through each other a third brane is produced stretching between them. We explain this phenomenon by the use of chains of dualities and the inflow of charge that is required for the absence of chiral gauge anomalies when pairs of D-branes intersect.Comment: 7 pages, two figure

Cell Competition: Pirates on the Tangled Bank

Competition by stem cells for occupation of a limited niche is a well-described phenomenon. Two recent studies highlight competition between hematopoietic stem cells based on p53. These findings have implications for both normal homeostasis and tumorigenesis

Autophagy and phagocytosis converge for better vision

The retinal pigment epithelium (RPE) is a single layer of nonregenerating cells essential to homeostasis in the retina and the preservation of vision. While the RPE perform a number of important functions, 2 essential processes are phagocytosis, which removes the most distal tips of the photoreceptors to support disk renewal, and the visual cycle, which maintains the supply of chromophore for regeneration of photo-bleached visual pigments. We recently reported that these processes are linked by a noncanonical form of autophagy termed LC3-associated phagocytosis (LAP) in which components of the autophagy pathway are co-opted by phagocytosis to recover vitamin A in support of optimal vision. Here we summarize these findings

p53 and Metabolism: Inside the TIGAR

The p53 tumor suppressor pathway coordinates DNA repair, cell-cycle arrest, apoptosis, and senescence to preserve genomic stability and prevent tumor formation. The discovery of three new target genes for p53 reveals unexpected functions for this tumor suppressor in the regulation of glucose metabolism and autophagy

The immune diet: meeting the metabolic demands of lymphocyte activation

During the adaptive immune response, lymphocytes undergo dramatic changes in metabolism that accompany the proliferative burst and differentiation into functional subsets. This brief overview focuses on recent advances in understanding the mechanisms of this metabolic reprogramming in T lymphocytes

Mitochondria and apoptosis: a quick take on a long view

Fifteen years of apoptosis research have led to the widely accepted idea that the major form of programmed cell death in mammals proceeds via the mitochondria, and that mitochondrial control of apoptosis is regulated by a specialized family of proteins known as the Bcl-2 family. Here we will consider some very recent data that has shed new insight into the regulation of these proteins and the impact of mitochondrial dynamics on mitochondrial outer membrane permeabilization (MOMP) and apoptosis

Innate Immune Recognition of mtDNA—An Undercover Signal?

In addition to their roles in cellular metabolism and apoptosis, mitochondria function as signaling platforms in the innate immune response. In Nature, West et al. (2015) demonstrate that mitochondrial stress triggers a type I interferon response and confers viral resistance via release of mtDNA and activation of the cGAS–STING pathway

Combinatorics of Boundaries in String Theory

We investigate the possibility that stringy nonperturbative effects appear as holes in the world-sheet. We focus on the case of Dirichlet string theory, which we argue should be formulated differently than in previous work, and we find that the effects of boundaries are naturally weighted by $e^{-O(1/g_{\rm st})}$.Comment: 12 pages, 2 figures, LaTe

Transforming Growth Factor β1 Inhibits Fas Ligand Expression and Subsequent Activation-induced Cell Death in T Cells via Downregulation of c-Myc

Activation-induced cell death (AICD) is a process that regulates the size and the duration of the primary immune T cell response. In this report, we investigated the mechanisms involved in the regulation of AICD by transforming growth factor β1 (TGF-β1). We found that TGF-β1 decreased apoptosis of human T cells or T cell hybridomas after activation by anti-CD3. This decrease was associated with inhibition of Fas (Apo-1/CD95) ligand (FasL) expression, whereas Fas signaling was not affected by TGF-β1. In parallel, TGF-β1 inhibited c-Myc expression in T cell hybridomas, and ectopic expression of a chimeric molecule composed of c-Myc and the steroid binding domain of the estrogen receptor (Myc-ER) blocked both the inhibition of FasL and the decrease of AICD induced by TGF-β1, providing that 4-hydroxytamoxifen was present. These results identify one mechanism by which TGF-β1 blocks AICD to allow the clonal expansion of effector T cells and the generation of memory T cells during immune responses