Buckets of beta cells - Nature Biotechnology; Multiple sclerosis genetics - Nature Genetics

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE - For papers published online on 25 September 2005

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

For papers that will be published online on 25 September 2005

Buckets of beta cells - Nature Biotechnology
Multiple sclerosis genetics - Nature Genetics

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********************NATURE BIOTECHNOLOGY***************************
(http://www.nature.com/naturebiotechnolgy)

[1] Buckets of beta cells

DOI: 10.1038/nbt1145

Transplantation of insulin-producing pancreatic beta-cells shows great
promise as a treatment for type 1 diabetes, but development of this therapy
is hampered by a severe shortage of donor beta-cells, which are obtained
from deceased human donors. In October's Nature Biotechnology, Kobayashi,
Yoon and colleagues describe a 'reversibly immortalized' cell line that can
supply large amounts of insulin-producing human beta-cells. Ultimately, a
cell line of this sort may provide an abundant source of beta-cells for
transplantation and an alternative to beta-cells from cadavers.
Type 1 diabetes results from the loss of insulin-producing beta-cells in the
pancreas. Because the supply of beta-cells from cadavers is insufficient to
meet the needs of 99% of diabetic patients, alternative sources of
beta-cells would be highly desirable. Previous efforts to coax mature human
beta-cells to survive and replicate in the laboratory have not succeeded,
however, because the cells died or lost their ability to produce insulin in
response to sugar stimulation.

Kobayashi, Yoon and colleagues got around this problem by manipulating and
analyzing large numbers of human beta-cells. First, they added genes that
extend cell lifespan to human beta-cells and looked for the rare cells that
did not form tumors and that expressed insulin and other beta-cell proteins.
Out of over 250 cell lines screened, only one passed this test. This cell
line was allowed to replicate to produce large numbers of cells. Then, the
genes that extend cell lifespan were removed to ensure that the cells would
not form tumors and to promote beta-cell behavior. The resulting cells
produced about 40% as much insulin as normal beta-cells and successfully
controlled blood sugar levels in diabetic mice for over 30 weeks.
Further research is needed before these cells can be considered for testing
in humans.

Author contact:
Ji-Won Yoon (Chicago Medical School, North Chicago, IL, USA)
Tel: +1 847 578 3436, E-mail: [email protected]

Additional contact for comment on paper:
Christopher Newgard (Duke University Medical Center, Durham, NC, USA)
Tel: +1 919 668 6059, E-mail: [email protected]

Other papers from Nature Biotechnology to be published online at the same
time and with the same embargo:

[2] Engineering the Fc region of immunoglobulin G to modulate in vivo
antibody levels
DOI: 10.1038/nbt1143

**********************NATURE GENETICS******************************
(<http://www.nature.com/naturegenetics>)

[3] & [4] Multiple sclerosis genetics

[3] DOI: 10.1038/ng1647 &
[4] DOI: 10.1038/ng1646

Two studies published in the October issue of Nature Genetics map genetic
regions associated with susceptibility to multiple sclerosis (MS). MS is a
prevalent autoimmune disorder of the central nervous system that leads to
inflammation and nerve damage and can result in progressive loss of motor
function. The disorder is believed to be caused by a combination of
environmental and genetic factors.

While no individual genes have been identified that lead to increased risk,
a large genetic region involved in immune recognition and response has
previously been associated with MS susceptibility. George Ebers and
colleagues now present a high-resolution map of this genetic region in
Canadian and Finnish individuals affected with MS. The authors refined the
boundaries for the genetic association and found that the primary risk is
associated with a class of genes involved in mediating immune reaction to
foreign proteins that cells take up from their environment.

In an accompanying study, David Reich and colleagues find evidence for a new
genetic influence on MS, using a computational strategy designed to find
risk variants that differ strikingly in frequency across human populations.
The study compared genetic regions in African American individuals with MS
versus healthy controls. The new computational approach used showed greater
power to detect weak factors contributing to disease risk than traditional
methods, and could be useful for identifying risk factors for other common
diseases such as lupus, end-stage renal disease and type 2 diabetes.

Author Contacts:
George C Ebers (University of Oxford, UK) - (paper no: [3])
Tel: +44 1865 228 579, E-mail: [email protected]

David Reich (Harvard Medical School, Boston, MA, USA) - (paper no: [4])
Tel: +1 617 432 6548, E-mail: [email protected]

Other papers from Nature Genetics to be published online at the same time
and with the same embargo:

[5] Apoptosis induced by vitamin A signaling is crucial for connecting the
ureters to the bladder
DOI: 10.1038/ng1645

[6] Identification of large ancient duplications associated with human gene
deserts
DOI: 10.1038/ng1648

[7] Mutations in SEPT9 cause hereditary neuralgic amyotrophy
DOI: 10.1038/ng1649

*****************************************************************
Items from other Nature journals to be published online at the same time and
with the same embargo:

NATURE MATERIALS (<http://www.nature.com/naturematerials>)

[8] Dynamics of field-driven domain-wall propagation in ferromagnetic
nanowires
DOI: 10.1038/nmat1477

[9] Residual stresses in thin polymer films cause rupture and dominate early
stages of dewetting
DOI: 10.1038/nmat1484

[10] Biphasic Janus particles with nanoscale anisotropy
DOI: 10.1038/nmat1486

[11] Aligned two- and three-dimensional structures by directional freezing
of polymers and nanoparticles
DOI: 10.1038/nmat1487

[12] Differential polymerization of the two main protein components of
dragline silk during fibre spinning
DOI: 10.1038/nmat1493

NATURE CHEMICAL BIOLOGY (<http://www.nature.com/nchembio>)

[13] Evolution of glutamate interactions during binding to a glutamate
receptor
DOI: 10.1038/nchembio738

Nature MEDICINE (<http://www.nature.com/naturemedicine>)

[14] Direct access to CD4+ T cells specific for defined antigens according
to CD154 expression
DOI: 10.1038/nm1292

[15] A live-cell assay to detect antigen-specific CD4+ T cells with diverse
cytokine profiles
DOI: 10.1038/nm1293

Nature IMMUNOLOGY (<http://www.nature.com/natureimmunology>)

[16] Essential function for the kinase TAK1 in innate and adaptive immune
responses
DOI: 10.1038/ni1255

[17] T cell receptor recognition of a 'super-bulged' major
histocompatibility complex class I-bound peptide
DOI: 10.1038/ni1257

NATURE CELL BIOLOGY (<http://www.nature.com/naturecellbiology>)

[18] ARHGAP10 is necessary for alpha-catenin recruitment at adherens
junctions and for Listeria invasion
DOI: 10.1038/ncb1308

[19] The focal adhesion scaffolding protein HEF1 regulates activation of the
Aurora-A and Nek2
kinases at the centrosome
DOI: 10.1038/ncb1309

Nature STRUCTURAL & MOLECULAR BIOLOGY
(<http://www.nature.com/natstructmolbiol>)

[20] MDC1 interacts with Rad51 and facilitates homologous recombination
DOI: 10.1038/nsmb991

[21] Sequential triage of transmembrane segments by Sec61alpha during
biogenesis of a native multispanning membrane protein
DOI: 10.1038/nsmb994

[22] CBP80 promotes interactions of Upf1 with Upf2 during nonsense-mediate
mRNA decay in mammalian cells
DOT: 10.1038/nsmb995

[23] Structure of the calcium-rich signature domain of human
thrombospondin-2
DOI: 10.1038/nsmb997

****************************************************************************
GEOGRAPHICAL LISTING OF AUTHORS

The following list of places refers to the whereabouts of authors on the
papers numbered in this release. The listing may be for an author's main
affiliation, or for a place where they are working temporarily. Please see
the PDF of the paper for full details.

AUSTRALIA
Brisbane: 17
Clayton: 17
Parkville: 17

BELGIUM
Antwerp: 7
Mons: 9

CANADA
Edmonton: 1
Montreal: 3
Vancouver: 3

FINLAND
Helsinki: 3
Kuopio: 7

FRANCE
Fort-de-France: 4
Gif-sur-Yvette: 18
Montpellier: 22
Mulhouse: 9
Nice: 18
Paris: 9, 18
Rennes: 4

GERMANY
Berlin: 14
Jena: 12
Muenster: 7

JAPAN
Fukuoka: 16
Kanagawa: 6
Kurashiki: 1
Kyoto: 1
Nagoya: 16
Okayama: 1
Okayama: 1
Suita: 16
Tokyo: 6
Yokahama: 6, 16

REPUBLIC OF KOREA
Gwangju: 1
Seoul: 22

REPUBLIC OF LEBANON
Beirut: 9

Islamic Republic of PAKISTAN
Faisalabad: 11

PORTUGAL
Porto: 18

SPAIN
Barakaldo: 7
Barcelona: 7

UNITED KINGDOM
Bebington: 11
Birmingham: 4
Liverpool: 11
Oxford: 3, 12
Sharnbrook: 11

UNITED STATES OF AMERICA
California
Los Angeles: 3
San Francisco: 4
Illinois
North Chicago: 1
Maryland
Bethesda: 15
Massachusetts
Boston: 1, 4, 20
Cambridge: 1,4, 5
Charlestown: 20
Michigan
Ann Arbor: 10
Detroit: 4
Missouri
St. Louis: 20
New York
New York: 5
Rochester: 22
North Carolina
Raleigh: 16
Oregon
Portland: 21
Pennsylvania
Philadelphia: 19
Texas
Austin: 8
College Station: 21
Dallas: 2, 5
Houston: 5, 13
Richardson: 2
Washington
Seattle: 7
Wisconsin
Madison: 23

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Laurie Dempsey
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Published: 25 Sep 2005

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