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Rockefeller University Press


Massive endocytosis in cells

Scientists identified a previously unknown mechanism for massive endocytosis (MEND) in cells, where up to 75% of the cell plasma membrane can be reversibly engulfed. MEND preferentially targets low-ordered, cholesterol-containing membrane domains.

SourceRockefeller University Press·JournalJournal of General Physiology·DateJan 17, 2011

With HMGB1's help, cells dine in

A team of researchers discovered HMGB1 as a critical pro-autophagic protein that enhances cell survival and limits programmed cell death. This finding suggests blocking HMGB1 could benefit cancer patients by preventing tumor cells from revving up autophagy to withstand chemotherapy, immunotherapy, and radiation treatment

SourceRockefeller University Press·JournalJournal of Cell Biology·DateSep 6, 2010

Tuning cocaine addiction

Reducing Ago2-dependent microRNA expression reduces cocaine consumption in mice, suggesting a link between genetic regulation and addiction. Further research is needed to determine which microRNAs control cocaine addiction and whether similar pathways operate in humans.

SourceRockefeller University Press·JournalJournal of Experimental Medicine·DateJul 19, 2010

Antagonizing atherosclerosis

Researchers found that antibody-producing B cells contribute to atherosclerosis in mice, while eliminating them could prevent the disease through increased production of immune protein interleukin-17. This discovery suggests that B cell-depleting drugs may also reduce the risk of atherosclerosis.

SourceRockefeller University Press·JournalJournal of Experimental Medicine·DateJul 5, 2010

Perspectives on computational biology methods

The Journal of General Physiology presents Perspectives on computational biology methods, including ab initio simulations and all-atom molecular dynamics. These approaches provide insights into membrane proteins and ion channels, highlighting the importance of multi-scale analysis in understanding physiological processes.

SourceRockefeller University Press·JournalJournal of General Physiology·DateMay 31, 2010

T cell protein boosts learning

A recent study discovered that a protein produced by T cells reduces inflammatory proteins hindering learning, improving navigation in mice trained to find their way through a water maze. Mice lacking this protein suffered from learning disabilities, which could be reversed with IL-4–producing T cells.

SourceRockefeller University Press·JournalJournal of Experimental Medicine·DateMay 3, 2010

Tackling blood stem cell heterogeneity

A study published in Journal of Experimental Medicine identifies distinct HSC populations with varying propensities to generate specific blood cell types. The research reveals that high CD150 expression is associated with a 'latent' or 'delayed' ability to generate new blood cells.

SourceRockefeller University Press·JournalJournal of Experimental Medicine·DateApr 26, 2010

New insight into Parkinson's disease

Parkin and PINK1 genes play a critical role in Parkinson's disease. The study found that PINK1 is rapidly degraded under healthy conditions, but its accumulation stabilizes at low membrane potential. Parkin is recruited to mitochondria with low potential to dispose of damaged organelles.

SourceRockefeller University Press·JournalJournal of Cell Biology·DateApr 19, 2010

Defective protein is a double hit for ataxia

A defective protein in spinocerebellar ataxia type 5 (SCA5) damages nerve cells by cutting the number of synaptic terminals and disrupting intracellular transportation. The study suggests that the complex containing beta-III-spectrin, dynactin, and dynein might also snag microtubules to prevent degeneration.

SourceRockefeller University Press·JournalJournal of Cell Biology·DateApr 5, 2010

TWEAK triggers atrophy of disused muscle

A study in JCB identifies TWEAK as a key trigger for muscle breakdown in disused skeletal muscle. Blocking this pathway could prevent muscle loss in immobilized patients. Inhibiting TWEAK with an antibody was sufficient to block muscle breakdown, suggesting its potential as a therapeutic target.

SourceRockefeller University Press·JournalJournal of Cell Biology·DateMar 22, 2010