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发表于 2011-5-5 23:53 |只看该作者 |倒序浏览 |打印

本帖最后由细胞海洋于 2011-5-6 00:17 编辑 0 m/ N! Y; U" B. p& _1 e& o

个人觉得搞干细胞还是应该关注一下其他领域的发展，所以在此上传一些2010年比较新比较火的领域的文献给大家分享。
这里有基础研究，临床研究，有结构生物学研究，希望对大家打开科研思维有所帮助。
目录：
1.[2010 Research]A Septin Diffusion Barrier at the Base of the Primary Cilium Maintains Ciliary Membrane Protein Distribution ! c: H1 \* @2 P  N# ?& K) {- G
Qicong Hu,1 Ljiljana Milenkovic,2,3 Hua Jin,4 Matthew P. Scott,2,3,5–8
Maxence V. Nachury,4 Elias T. Spiliotis,9* W. James Nelson1,4*$ q7 c2 ]/ J  N8 n  x

In animal cells, the primary cilium transduces extracellular signals through signaling receptors
localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the8 E5 p0 l. c  h$ G: G
cilium is unknown. We found that ciliary membrane proteins were highly mobile, but their
diffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member- N9 Z; z/ m5 [- P( O& @
of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast,6 u* ~7 F' q+ h2 G
localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane+ b% E3 r- N% W4 L2 P$ [
protein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus,
SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for
retaining receptor-signaling pathways in the primary cilium.+ Q7 C- ^2 P8 H% U
2. [2010 Research]Cancer Statistics
3. [2010 Research]Dendritic Cells in Systemic Lupus Erythematosus
Heather M. Seitz
Johnson County Community College, Science Division, Overland Park,
Kansas, USA
Glenn K. Matsushima* @) y6 _8 ]; v" c% a& D
UNC Neuroscience Center, Department of Microbiology & Immunology,
Program for Molecular Biology & Biotechnology, University of North
Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
; r  b: s8 s3 o( I
Systemic lupus erythematosus (SLE) persists as a chronic inflammatory autoimmune
disease and is characterized by the production of autoantibodies4 e% H: \; D: w
and immune complexes that affect multiple organs. The underlying mechanism1 r6 O' ?9 P" ]  f" T. c8 n: f
that triggers and sustains disease are complex and involve certain
susceptibility genes and environmental factors. There have been several immune5 `1 ?6 M0 A. I1 x( E5 M
mediators linked to SLE including cytokines and chemokines that have) Y: Y: S& Y- k
been reviewed elsewhere [1–3]. A number of articles have reviewed the role
of B cells and T cells in SLE [4–10]. Here, we focus on the role of dendritic
cells (DC) and innate immune factors that may regulate autoreactive B cells.
4. [2010 Research]Differential immunophenotypic analysis of dendritic cell tumours
Tomohiko Orii,1,2 Hiroaki Takeda,2 Sumio Kawata,2 Kunihiko Maeda,1
Mitsunori Yamakawa1

ABSTRACT5 V- {" I- J7 p! q3 r
Aims The phenotypic and biological characteristics of
dendritic cell (DC) tumours have not been fully1 E  `; Z! k1 q, H
elucidated. The aim of this study was to compare the
immunophenotypic characteristics of DC-related markers, {) T9 F* Y3 K' o0 z
and cell-cycle-associated markers among DC tumours& N, J- m5 R- |1 v$ q' I. e: {$ j
and finally to utilise them for differential diagnosis of DC/ h" w8 ^6 n% @2 |5 n
tumours.' W; _8 }5 C) z7 u
Methods Tissue sections from 28 patients with DC
tumours were immunohistochemically examined using5 Y. y1 O' z; M% U5 |
DC-related and cell-cycle-associated markers.
Results The Langerhans cell histiocytosis (LCH) and+ C0 s) A* C! I3 C! W
Langerhans cell sarcoma (LCS) samples were positive for: S, C) `$ Z' Y8 n, `
S-100 protein, CD1a, Langerin, fascin, DEC-205 and DCSIGN., _1 ]6 G" `. t7 a
Interdigitating dendritic cell sarcoma (IDCS) was
positive for S-100 protein and fascin and negative for! S6 `8 E4 i! E) i
Langerin. In addition, two IDCS samples were positive for9 N% c% n) v( S* i. ~4 v
CD1a, DEC-205 and DC-SIGN. The labelling indices of
Ki-67, cyclin A, cyclin B1 and acetylated histone H3 on the
LCS and IDCS specimens were significantly higher than
those on the LCH specimens. The expression of p53 was
also significantly higher in the LCS specimens than in the4 V% P& Z' ]) ^' _, w8 Y. ]
LCH specimens. The numbers of infiltrating CD123+ and' W/ j& Q3 e% X: w% V7 v
FOXP3+ cells were also significantly higher in the LCS" M" L% W# x* b! @
samples than in the LCH and IDCS samples. Follicular$ E/ A1 X) R3 X) I
dendritic cell sarcoma was distinguished from other DC6 B5 L9 D0 ^1 }7 z
tumours by the lack of DC-SIGN, Langerin and DCE-205.
Conclusions These results suggest that Langerin can be1 s! i! @" m0 O$ j- n
used to distinguish LCS from IDCS, and DC-SIGN and' F3 H, E- w6 B6 Y. @, d3 C& ^
DEC-205 can be used to identify DC tumour cells. The
frequency of cell-cycle-associated markers can be used: L2 r0 p, {! j1 ^' T" ^7 p
for the differential diagnosis of malignant and benign DC tumours.8 W( r0 W/ B" M" u
5. [2010 Research]Gut inflammation provides a respiratory electron acceptor for Salmonella3 T* O/ N7 U, a* O7 l5 L
Sebastian E. Winter1, Parameth Thiennimitr1,2, Maria G. Winter1, Brian P. Butler1, Douglas L. Huseby3, Robert W. Crawford1,
Joseph M. Russell1, Charles L. Bevins1, L. Garry Adams4, Rene′e M. Tsolis1, John R. Roth3 & Andreas J. Ba¨umler1% O% h) D- T9 k/ W% }+ r

Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence
factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response9 {' U. z- r3 t9 y+ Z/ a9 E2 Y2 W
enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through8 W, [8 L2 X9 k* {
unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with
endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate.1 E+ v+ G7 m9 g: r
The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S.
Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium
virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use3 ^' d6 R8 \$ g% W1 O
respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for* t3 h, Q& h6 X9 }
the biology of this diarrhoeal pathogen.
6. [2010 Research]Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels& ?1 Y+ }7 h( \
Bertrand Coste,1 Jayanti Mathur,2 Manuela Schmidt,1 Taryn J. Earley,1 Sanjeev Ranade,1: E+ M; \' S. h
Matt J. Petrus,2 Adrienne E. Dubin,1 Ardem Patapoutian1,2*0 X* s. E; `( I6 }
" u0 b" l' _% c0 N
Mechanical stimuli drive many physiological processes, including touch and pain sensation,
hearing, and blood pressure regulation. Mechanically activated (MA) cation channel activities
have been recorded in many cells, but the responsible molecules have not been identified.% h& c  `9 T* @7 H# [( d
We characterized a rapidly adapting MA current in a mouse neuroblastoma cell line. Expression
profiling and RNA interference knockdown of candidate genes identified Piezo1 (Fam38A) to be
required for MA currents in these cells. Piezo1 and related Piezo2 (Fam38B) are vertebrate3 G1 a, x0 v& ]2 u) |2 s1 d1 p
multipass transmembrane proteins with homologs in invertebrates, plants, and protozoa.
Overexpression of mouse Piezo1 or Piezo2 induced two kinetically distinct MA currents. Piezos% U9 ]3 B) [% o. Y# a
are expressed in several tissues, and knockdown of Piezo2 in dorsal root ganglia neurons
specifically reduced rapidly adapting MA currents. We propose that Piezos are components of5 v/ {; g. z3 t1 Q
MA cation channels.
7. [2010 Research]Platelets Amplify Inflammation in Arthritis via Collagen-Dependent Microparticle Production+ z9 J) m# k6 y5 y
Eric Boilard,1 Peter A. Nigrovic,1,2 Katherine Larabee,1 Gerald F. M. Watts,1
Jonathan S. Coblyn,1 Michael E. Weinblatt,1 Elena M. Massarotti,1& O" d7 U5 N- l% F) S+ v3 t# \
Eileen Remold-O’Donnell,3 Richard W. Farndale,4 Jerry Ware,5 David M. Lee1*

In addition to their pivotal role in thrombosis and wound repair, platelets participate in2 _: ~) l- b7 @( t
inflammatory responses. We investigated the role of platelets in the autoimmune disease* ^% Z4 n* J+ ?1 R: ^- w  l
rheumatoid arthritis. We identified platelet microparticles—submicrometer vesicles elaborated by3 R  s" C' h3 s7 {$ ~
activated platelets—in joint fluid from patients with rheumatoid arthritis and other forms of
inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet7 t) `, A% H/ u8 [! u+ f5 f& f7 r
microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via
interleukin-1. Consistent with these findings, depletion of platelets attenuated murine
inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the
collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis
pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets5 u* s2 v& K6 Z' w
and their activation-induced microparticles in inflammatory joint diseases.. R) D+ z' }* O" r: H5 q2 _5 K+ _
8. [2010 Research]The architecture of respiratory complex I
Rouslan G. Efremov*, Rozbeh Baradaran* & Leonid A. Sazanov# N9 K8 g+ L) v' I

Complex I is the first enzyme of the respiratory chain and has a central role in cellular energy production, coupling electron* Z% `) H" m4 U1 M' Y$ t! }2 j
transfer between NADH and quinone to proton translocation by an unknown mechanism. Dysfunction of complex I has been
implicated in many human neurodegenerative diseases. We have determined the structure of its hydrophilic domain( d2 l$ P' T( P% C
previously. Here, we report the a-helical structure of the membrane domain of complex I from Escherichia coli at 3.9A°' z  |: p6 p, l2 f/ I4 R. ~
resolution. The antiporter-like subunits NuoL/M/Neach contain 14 conserved transmembrane (TM) helices. Two of them are1 Q  ]9 a+ B9 u2 O3 z0 G
discontinuous, as in some transporters. Unexpectedly, subunit NuoL also contains a 110-A° long amphipathic a-helix, spanning
almost the entire length of the domain. Furthermore, we have determined the structure of the entire complex I from Thermus# P& ]* E+ r$ x& s: y3 [: p9 F
thermophilus at 4.5A°
resolution. The L-shaped assembly consists of the a-helicalmodel for themembrane domain, with 63TM, d- R, V3 \, ?
helices, and the known structure of the hydrophilic domain. The architecture of the complex provides strong clues about the
coupling mechanism: the conformational changes at the interface of the two main domains may drive the long amphipathic0 G* X; x3 |0 _& I* U3 O. Q$ b
a-helix of NuoL in a piston-like motion, tilting nearby discontinuous TM helices, resulting in proton translocation.
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