As human cells begin to divide, their
chromosomes align in the center, attached to poles at each end of the cell
by structures called spindles, which are made up of small fibers called
microtubules. The spindles maintain constant length by simultaneously
building up one end while disassembling the other. New research from Tarun Kapoor’s
Laboratory of Chemistry and Cell Biology has now identified how three
proteins regulate the length of these spindles by playing a role in the
disassembly of microtubule fibers. Using confocal fluorescence microscopy
and fluorescent speckle microscopy, the researchers observed in real time
that the microtubules, and therefore the spindles, lengthen when the
proteins — dynein, dynactin and NuMA — are inhibited. The
finding suggests that the three proteins regulate spindle length by helping
a fourth protein, called Kif2a, target the appropriate end of the spindle.
Journal of Cell Biology,
August 16, 2004
Improved therapy for amyloidosis. People with primary systemic
amyloidosis, a disease of the bone marrow, develop deposits of protein
fibers called amyloid, similar to those in the brains of Alzheimer’s
patients, throughout their organs and tissues. Unlike Alzheimer’s,
the disease kills quickly — median survival time is only 13 months.
Now a team of researchers led by Madhav Dhodapkar has shown that treatment with
drugs already used for multiple myeloma can more than double the survival
time of amyloidosis patients. Between 1996 and 2003, the researchers
treated 87 patients with high dose dexamethasone, and then maintained them
on a regimen of dexamethasone and another myeloma drug, alpha-interferon.
The patients survived for an average of 31 months. The study paves the way
for dexamethasone becoming a standard therapy for amyloidosis. Dhodapkar is
head of the Laboratory of Tumor Immunology and Immunotherapy.
Blood, August 12, 2004
How TB hides. Tuberculosis
remains a threat long after the initial infection because the bacterium,
M. tuberculosis, that causes it
has evolved effective ways of dodging the immune system’s attacks.
Research in both animals and humans has implicated a chemical messenger
called gamma-interferon as a key weapon in immune system cells. Now, using
a genetic screening technique known as differential signature-tagged
transposon mutagenesis, which involves creating mutant TB strains and
testing their virulence in immune-deficient mice, researchers in John McKinney’s Laboratory
of Infection Biology have identified three M.
tuberculosis genes used to repel the
attacks driven by gamma-interferon. The researchers suggest that
understanding TB’s immune evasion strategies could result in drugs
that boost the immune system’s effectiveness against TB.
Infection and Immunity, September
July 16, 2004
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