AUGUSTA, Ga. — A diametric shift in the levels of two proteins involved in folding, moving and cutting other proteins enables accumulation of the destructive brain plaque found in Alzheimer’s disease, researchers report.
VPS35 is a protein that fold…
Tag Archives | journal of cell biology
Diametric shift in 2 protein levels spurs Alzheimer’s plaque accumulation
Macho muscle cells force their way to fusion
In fact, according to new research from Johns Hopkins, the fusion of muscle cells is a power struggle that involves a smaller mobile antagonist that points at, pokes and finally pushes into its larger, stationary partner using a newly identified …
Expanding drug development horizons: Receptor behaviors observed in living cell membranes
Kyoto, Japan — Unprecedented single molecule imaging movies of living cell membranes, taken by a research team based at Kyoto University and the University of New Mexico, have clarified a decades-old enigma surrounding receptor molecule behaviors. …
Chaperone enzyme provides new target for cancer treatments
UNC scientists who study how cells repair damage from environmental factors like sunlight and cigarette smoke have discovered how a “chaperone” enzyme plays a key role in cells’ ability to tolerate the DNA damage that leads to cancer and other disea…
Trigger mechanism provides ‘quality control’ in cell division
SALT LAKE CITY, November 22, 2010 — Researchers from Huntsman Cancer Institute (HCI) at the University of Utah report that they have identified a previously undiscovered trigger mechanism for a quality control checkpoint at the very end of the cel…
‘Reaper’ protein strikes at mitochondria to kill cells
Our cells live ever on the verge of suicide, requiring the close attention of a team of molecules to prevent the cells from pulling the trigger. This self-destructive tendency can be a very good thing, as when dangerous precancerous cells are permit…
Researchers define role of CEP290 in maintaining ciliary function
A new study in the September 6 issue of the Journal of Cell Biology (www.jcb.org) helps define the role of an important ciliary protein, CEP290. The results could be applied toward targeted gene therapy in cilia-related diseases.
Mutations in hu…
With HMGB1′s help, cells dine in
Like some people, cells eat when they are under pressure — but they consume parts of themselves. A multi-function protein helps control this form of cannibalism, according to a study in the September 6 issue of the Journal of Cell Biology (ww…
Alzheimer's protein jams mitochondria; resulting 'energy crisis' kills neurons
Opening a new front in the battle against Alzheimer’s disease, scientists at the University of Pennsylvania have found that a protein long associated with the disease inflicts grave damage in a previously unimagined way: It seals off mitochondria in affected neurons, resulting in an “energy crisis” and buildup of toxins that causes cells to die. This pathway, the first specific biochemical explanation for pathologies associated with Alzheimer’s, is detailed in the April 14 issue of the Journal of Cell Biology.
Abnormal Number of Chromosomes is One Step in Cancer Development
Researchers have produced the first laboratory evidence to show that a cell’s possession of an abnormal numbers of chromosomes contributes to the development of cancers. Their report on the role of this chromosomal instability, known as aneuploidy, appears in today’s online edition of the Feb. 3 Journal of Cell Biology. Because 85 percent of human cancer cells possess an abnormal number of chromosomes, researchers have long been curious about the role of aneuploidy in the multistep cancer process.
Cancer squeezes through the gaps
Cancer cells move around the body (become metastatic) by chopping up the dense matrix that surrounds them. But drugs that prevent the chopping have been disappointing in animal and human anti-cancer trials. Now researchers provide an explanation for this failure: the drug-treated cells revert to a primordial, ameboid form of cell movement that allows them to squeeze through gaps in the matrix.
Cell keeps spare set of DNA to ensure offspring gets fresh start
This is a little complex, but bear with us. Nearly all cells house their DNA inside a nucleus. But a little one-celled critter called Tetrahymena houses different versions of its DNA in each of its two nuclei. Researchers have found that the smaller nucleus (called the micronucleus) just keeps the cell’s full genome safe, acting as a sort of “lock box.” The larger nucleus (called the macronucleus) uses the DNA to regulate the cell’s life functions. When the cell mates to create a new generation, the two work together to compare the cell’s current DNA against what’s been stored in the lock box. If any foreign genes have snuck in (like from a virus) they nuclei eliminate it, to make sure baby gets a fresh start. Pretty neat, with possible implications for larger organisms, too.
Fat cells converted to bone
Pre-cells destined to become fat can be converted instead into true bone cells in
response to outside signals, say researchers at the University of California, San Francisco. The finding could pave the way for scientists to replenish lost bone cells in patients with conditions like osteoporosis, and to help repair bone defects. The new bone cells have all the hallmarks associated with mature bone formation, including production of bone proteins and calcification, the UCSF team says.