Skin cells that have lost their luster flake off and are replaced by new ones that push their way up to the surface. In new research that further dissects how stem cells specialize into tissue cells, scientists now show how these new skin cells arise — work that may one day hold promise for burn victims. More »
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Glands and Ducts Reveals Roles in Homeostasis and Wound Repair
Herpes in STAT1 deficiency
Scale invariance in the dynamics of spontaneous behavior
Mechanistic basis for low threshold mechanosensitivity in voltage-dependent K+ channels
Tiki1 Is Required for Head Formation via Wnt Cleavage-Oxidation and Inactivation
Apoptotic and antitumor activity of death receptor antibodies require inhibitory Fcγ receptor engagement
Mouse model of endemic Burkitt translocations reveals the long-range boundaries of Ig-mediated oncogene deregulation
Telomere-driven tetraploidization occurs in human cells undergoing crisis and promotes transformation of mouse cells
Dynamics of TGF-β signaling reveal adaptive and pulsatile behaviors reflected in the nuclear localization of transcription factor Smad4
dSarm/Sarm1 Is Required for Activation of an Injury-Induced Axon Death Pathway
Contingency and statistical laws in replicate microbial closed ecosystems
Expression of the zinc finger transcription factor zDC (Zbtb46, Btbd4) defines the classical dendritic cell lineage



Radio-wave heating of iron oxide nanoparticles can regulate plasma glucose in mice



Viral-induced encephalitis initiates distinct and functional CD103+ CD11b+ brain dendritic cell populations within the olfactory bulb

















The pores that control what passes in and out of the cell nucleus play a crucial role in the cell’s metabolism and signaling. Defects in structure and function of these gatekeepers, known as nuclear pore complexes, can have lethal consequences. New research reveals secrets about what may be a key design feature of these structures, a flexibility enabling the import and export of large molecules.
New research suggests that anthrax-causing bacteria work synergistically with viruses to extend each other’s life spans. The work puts scientists on a new playing field in the fight against biological warfare and antibiotic-resistance, and also calls into question the degree to which our genomes are the sole masters of our fates.
How a handful of social animals ever learned to actively style their vocal communication is a question that has dogged biologists for generations. New research in chipping sparrows suggests that the talent originally appeared in these songbirds as a competition for food among siblings and later evolved into vocal imitation used in territorial defense and courtship.
In the developing brain, generations of young neurons undergo a staged migration, with the earliest-born cells staying relatively close to their birthplace and subsequent generations traveling further, ultimately stratifying into six neuronal layers in the mature brain. For the first time, imaging studies have identified the “motors” that propel this unique form of cell migration, giving insight into the delicate layering of the brain that underlies the formation of synaptic circuitry.
Bacteria know that they are too small to make an impact individually. So they wait; they multiply, and then they engage in behaviors that are only successful when all cells participate in unison. There are hundreds of behaviors that bacteria carry out in such communities. Now researchers have discovered that bacteria form an unusual solitary wave, a behavior that has never been observed or described before in a living system.
Although telomeres are fragile, they don’t have to be handled with care. Researchers at Rockefeller University now show that what keeps our fragile telomeres from falling apart is a protein known as TRF1 that ensures the smooth progression of DNA replication to the end of a chromosome. The work not only shows how telomeres help chromosomes protect their vulnerable ends but also reveals how the genome is made more stable by them.
Cells use bubbles called vesicles to ferry cargo to and from the membrane. Scientists long believed that this importing and exporting were independent processes. But by imaging individual vesicles as they are fusing with the cell membrane, researchers reveal that these processes have a lot in common: Certain molecules handle cargo moving in both directions.
MicroRNAs are the newest kid on the genetic block. By regulating the unzipping of genetic information, these tiny molecules have set the scientific world alight with their therapeutic potential and wide-ranging applications. But the question remains: How do they work? By using a technique that molecularly cements proteins to RNAs, Rockefeller scientists have decoded a map of microRNA-messenger RNA interactions in the mouse brain, an advance that holds promise for biology and human disease.
The development of blood from stem cell to fully formed blood cell follows a genetically determined program. When it doesn’t work properly, genetic mutations can cause the developing cells to turn cancerous. In research published in the journal Nature, Rockefeller University scientists show for the first time that a misreading of blood cells’ histone code is responsible for acute myeloid leukemia, a rare form of the deadly blood cancer. 


