These short, accessible highlights summarize and contextualize must-read papers related to cell signaling. These articles add background and context to summaries of primary research. 'In brief' articles emphasize key aspects of selected articles.
 | Dopamine pathway: ETS make a neuron
The ETS family of transcription factors bind to a conserved cis-regulatory element in dopamine responsive genes to promote neuronal differentiation.
Original research paper: Nature 458, 885-889 (2009) |
 | Neural development: Proteoglycans go forth to multiply
Sonic hedgehog requires interactions with proteoglycans to achieve cell proliferation, but not tissue patterning.
Original research paper: Nature Neuroscience 12, 409-417 (2009) |
 | Protein kinase D1: A (sling)shot against directed migration
PKD1 inhibits the activation of cofilin at the cell front via slingshot phosphatases, thus blocking the formation of free F-actin barbed ends and directed cell migration.
Original research paper: Nature Cell Biology 11, 545-556 (2009) |
 | Energy homeostasis: AMPing up SIRT1
AMPK responds to energy deprivation by increasing cellular NAD+ levels, which activates SIRT1 and stimulates transcription of genes important for mitochondrial biogenesis and fatty-acid oxidation.
Original research paper: Nature 458, 1056-1060 (2009) |
 | In brief: April 2009
DNA damage response | 2010 Mechanotransduction | Metabolism | Therapeutics | Synaptic plasticity | Neurodegenerative disease | Wound repair | Immune regulation | Microscopy | Proteomics |
 | Cell migration: Cells go A-B-C
ATP-binding cassette (ABC) transporters export lipid-modified peptides that are essential for directed cell migration.
Original research paper: Science 323, 943-946 (2009) |
 | Immune regulation: DAMPening inflammation
The CD24-SiglecG pathway selectively represses the NF-κB-driven inflammatory response to danger-associated molecular patterns (DAMPs) but not pathogen-associated molecular patterns (PAMPs), suggesting that this pathway might be a general mechanism to distinguish between tissue injury and infection.
Original research paper: Science 323, 1722-1725 (2009) |
 | Metastasis: Oxidizing abnormalities
The oxygen-sensitive prolyl hydroxylase Phd2 regulates endothelial cell morphology, which consequently modifies the aggressiveness of tumors.
Original research paper: Cell 136, 839-851 (2009) |
 | Resistance: Aggravating the aggressor
Increased Akt activity in glioblastoma multiforme appears to be associated with the acquisition of stem cell-like properties and therapeutic resistance.
Original research paper: Cell Stem Cell 4, 226-235 (2009) |
 | Neurodegenerative disorders: Reversing the impairment
Therapeutic delivery of brain-derived neurotrophic factor (BDNF) to the entorhinal cortex can ameliorate many of the hallmarks of Alzheimer's disease without directly modulating amyloid-β.
Original research paper: Nature Med. 15, 331-337 (2009) |
 | Plant cell biology: When autumn falls
Age-dependent senescence in Arabidopsis thaliana leaves is regulated by three components of a feed-forward loop — ORESARA 1 (ORE1), ETHYLENE INSENSITIVE 2 (EIN2) and the microRNA miR164.
Original research paper: Science 323, 1053-1057 (2009) |
 | Cell death and immunity: CLEC9A: linking necrosis and immunity
CD8α+ dendritic cells (DCs) express the C-type lectin receptor CLEC9, which couples necrotic cell recognition to the subsequent cross-presentation of dead-cell-associated antigens to T cells.
Original research paper: Nature 458, 899-903 (2009) |
 | Insertional Mutagenesis: Flip'in beautiful
A tissue-specific version of the Sleeping Beauty (SB) transposon can be used to develop mouse models of human tumors and identify new oncogenes or tumor suppressors.
Original research paper: Nature Biotech. 27, 264-274 (2009) |
 | Development and disease: Alzheimer's protein in embryonic pruning
Embryonic neuronal connections are refined by amyloid precursor protein (APP) signaling through the death receptor DR6, which may also have a role in the development of Alzheimer's disease.
Original research paper: Nature 457, 981-989 (2009) |
 | Muscular dystrophy: Fixing the leak
A defect in the skeletal muscle ryanodine receptor (RYR1) may contribute to the deregulated Ca2+ homeostasis and muscle damage typical of Duchenne muscular dystrophy (DMD), suggesting that it could be a new therapeutic target for this disease.
Original research paper: Nature Med. 15, 325-330 (2009) |
 | Regulatory T cells: Fine-tuning TReg cells
During chronic hepatitis C virus (HCV) infection the behavior of TReg cells is fine-tuned through a negative regulatory mechanism involving programmed cell death 1 (PD1).
Original research paper: J. Clin. Invest. 119, 551-564 (2009) |
 | Migration: Calcium influx is moving
ORAI1 and STIM1 have a known role in regulating store-operated Ca2+ influx in non-excitable cells, and have now been shown to facilitate cell migration by regulating focal adhesion turnover.
Original research paper: Cancer Cell 15, 124-134 (2009) |
 | Development: Linking the loops for digit identity
Researchers have used mathematical modeling to complement genetic screening in a bid to understand the genetic interactions and kinetics of feedback loops in mammalian limb development.
Original research paper: Science 323, 1050-1053 (2009) |
 | Neurodegenerative disease: Orphan receptor coupled to Aβ production
The orphan G-protein-coupled receptor GPR3 has been validated as a potential new therapeutic target for the treatment of Alzheimer's disease.
Original research paper: Science 323, 946-951 (2009) |
 | Protein biochemistry: Snapshots of proteins at work
The use of in-cell nuclear magnetic resonance spectroscopy has enabled the generation of high-quality structures of proteins at work within cells.
Original research paper: Nature 458, 102-105 (2009) |
 | Cytoskeleton: N-WASP turnover: the sting in the actin tail
Viral actin-based motility is regulated by the rate of N-WASP turnover during ARP2/3-complex-dependent actin polymerization.
Original research paper: Nature 458, 87-91 (2009) |
 | T-cell responses: Directing responses in death
Dendritic cells that engulf apoptotic cells direct the generation of either TH17 or TReg cells depending on whether Toll-like receptor (TLR) ligands are present or absent in the dying cells.
Original research paper: Nature 458, 78-82 (2009) |
 | Metastasis: CHIPping away at tumour progression
Reduced levels of the ubiquitin ligase CHIP result in the accumulation of SRC3, a transcriptional co-activator that controls the transcription of proteins involved in the epithelial–mesenchymal transition (EMT).
Original research paper: Nature Cell Biol. 11, 312-319 (2009) |
 | Signal transduction: Deleting PTEN for better or worse
Two studies show that PTEN (phosphatase and tensin homolog) and its downstream signaling pathway might be promising targets for treatments aimed at boosting neural stem cell proliferation in neurodegenerative diseases and at reversing the symptoms of some neurodevelopmental disorders.
Original research paper: J. Neurosci. 29, 1773-1783 (2009) |
 | Innate immunity: Not-so-lucky 7 for West Nile virus
Brain-resident macrophages detect West Nile virus single-stranded RNA through Toll-like receptor 7 (TLR7), leading to the secretion of high levels of interleukin-23 and the attraction of infiltrating macrophages and other leukocytes that neutralize and clear the infection.
Original research paper: Immunity 30, 242-253 (2009) |
