2010 Some Hot Research & Report Papers

清风闲云

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) o* y7 ?/ @& C2 V4 A; o1 q+ U% Z$ f; w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。0 ^/ T2 p( y. ?+ O
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。" P: U% W0 U# F+ W7 z, _
目录：
3 Z; ~1 l- O( x; E1.[2010 Research]A Septin Diffusion Barrier at the Base of the Primary Cilium Maintains Ciliary Membrane Protein Distribution ' ^) Z8 V" c; c0 z3 A- \$ ^* U2 z
Qicong Hu,1 Ljiljana Milenkovic,2,3 Hua Jin,4 Matthew P. Scott,2,3,5–8
: T. G  D. o! P5 {$ k, ~- WMaxence V. Nachury,4 Elias T. Spiliotis,9* W. James Nelson1,4*
$ R3 C( P7 P) D2 f; ^6 @' W# K; f: T: D  `3 P, Z- x- N; W
In animal cells, the primary cilium transduces extracellular signals through signaling receptors
2 ?) T7 H2 t% t) i& wlocalized in the ciliary membrane, but how these ciliary membrane proteins are retained in the
& \# }2 v* Y( s5 Acilium is unknown. We found that ciliary membrane proteins were highly mobile, but their" Y$ B; q( m& m6 Z$ a) M
diffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member& [# w# w- R) g' u, t( T( t& q
of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast,8 T7 O% C" u' P2 k+ E$ @! M, u. k, r
localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane
- [: _7 d) ]- R( fprotein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus,9 g2 \+ Y) N, y% u1 n
SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for9 A, x+ E( R, r0 o( h
retaining receptor-signaling pathways in the primary cilium.
* G9 {) w( z+ E& G1 b2. [2010 Research]Cancer Statistics
8 x. \7 s# F% W% k8 k6 f  l$ t3. [2010 Research]Dendritic Cells in Systemic Lupus Erythematosus( u, X9 a2 F4 ^( B
Heather M. Seitz/ ~8 U4 x, B) I6 V
Johnson County Community College, Science Division, Overland Park,* _4 A! ]3 f; M# d+ N, W5 Y7 `. h
Kansas, USA, x$ Y7 Q  }# |, s9 K
Glenn K. Matsushima
/ l/ Z/ q& ?# v$ H2 CUNC Neuroscience Center, Department of Microbiology & Immunology,) [1 i+ l9 w* \( {! A5 a7 I
Program for Molecular Biology & Biotechnology, University of North
9 a  ?* R9 C3 i# V. Y) _' JCarolina at Chapel Hill, Chapel Hill, North Carolina, USA
. w3 z, x: X2 v( t! g5 K3 G
6 @0 H) i4 C- R8 ~  h1 K/ BSystemic lupus erythematosus (SLE) persists as a chronic inflammatory autoimmune5 z0 r: @) ^* A& U3 B4 A& Q9 z3 o
disease and is characterized by the production of autoantibodies
" l( _+ p/ T* m5 F2 Jand immune complexes that affect multiple organs. The underlying mechanism
# j) D# [. I( N( z& Y1 athat triggers and sustains disease are complex and involve certain
) O3 i; [3 l) G+ y; y3 n9 J  v9 [susceptibility genes and environmental factors. There have been several immune: |& D4 y/ O" M( u. m, [6 Z  d: h5 |1 V
mediators linked to SLE including cytokines and chemokines that have
- m) r( Y+ J% X7 I$ g% Gbeen reviewed elsewhere [1–3]. A number of articles have reviewed the role3 t, ~- S0 B% _& b2 ~7 @
of B cells and T cells in SLE [4–10]. Here, we focus on the role of dendritic
; q# J7 @  F; r' n7 Rcells (DC) and innate immune factors that may regulate autoreactive B cells.
' Y/ m! `% f5 Q* J4. [2010 Research]Differential immunophenotypic analysis of dendritic cell tumours
% l) ~$ @3 m: h* }* r& ITomohiko Orii,1,2 Hiroaki Takeda,2 Sumio Kawata,2 Kunihiko Maeda,1
/ G0 t0 b' Z; RMitsunori Yamakawa17 I6 Q8 m& c+ O( Z: F" W
& [% T  a+ y5 b/ |# K, D
ABSTRACT
6 k- O; r7 p% \, G( {: ~! b# CAims The phenotypic and biological characteristics of) }' V; B1 C# Z0 s+ @2 J8 O
dendritic cell (DC) tumours have not been fully
% r- W- I0 ?1 t5 M9 M+ V( e5 Qelucidated. The aim of this study was to compare the# ]; T1 {0 e/ a% [% t' P: U5 P) M! {
immunophenotypic characteristics of DC-related markers" `, R6 v0 Y, `' Y) c+ x4 l" U
and cell-cycle-associated markers among DC tumours. `! a6 G/ Z3 d" q3 S# r
and finally to utilise them for differential diagnosis of DC
! {8 n! S% S$ g0 f$ d# U5 Htumours.
+ s7 a4 j$ y" ?9 J! uMethods Tissue sections from 28 patients with DC
) J! U, E0 C/ p- stumours were immunohistochemically examined using6 z7 o1 F6 o" l* `' e' ^. m: r8 V
DC-related and cell-cycle-associated markers.
' r' Y7 l& f$ _Results The Langerhans cell histiocytosis (LCH) and5 I+ v9 x2 @6 B/ G6 y
Langerhans cell sarcoma (LCS) samples were positive for- e+ A/ @0 A% u- \/ k& D
S-100 protein, CD1a, Langerin, fascin, DEC-205 and DCSIGN.  J3 ~6 ~! H' }2 T1 f
Interdigitating dendritic cell sarcoma (IDCS) was
  }$ S+ Q1 }% fpositive for S-100 protein and fascin and negative for4 D" T0 Z: |* n* ^0 @; I) k; t$ m
Langerin. In addition, two IDCS samples were positive for. G# J1 z4 R: m) t4 P
CD1a, DEC-205 and DC-SIGN. The labelling indices of. Q8 L" K8 m+ g
Ki-67, cyclin A, cyclin B1 and acetylated histone H3 on the# p9 y. ~3 ]- ?  [" f* I% E
LCS and IDCS specimens were significantly higher than' q, N6 @! x8 H9 H& k* R9 W: [
those on the LCH specimens. The expression of p53 was
( S# t3 H5 n8 J8 R+ R! [6 R* Salso significantly higher in the LCS specimens than in the
9 k" ~: ]; e9 K) \' W/ JLCH specimens. The numbers of infiltrating CD123+ and
4 ?* k$ Z7 x( K5 e  vFOXP3+ cells were also significantly higher in the LCS
& l! J( |8 m- s* fsamples than in the LCH and IDCS samples. Follicular5 ?- @6 G- v! w
dendritic cell sarcoma was distinguished from other DC
- a5 \/ ]* R1 |& c/ i/ |. k5 O8 Itumours by the lack of DC-SIGN, Langerin and DCE-205.. b3 t, D  y3 L: W& x9 t9 S
Conclusions These results suggest that Langerin can be
0 I6 |# z. Z. U; v7 W! k4 i( w+ }used to distinguish LCS from IDCS, and DC-SIGN and$ @& A/ z8 K8 S' V
DEC-205 can be used to identify DC tumour cells. The" Z( }9 c1 x$ f2 x7 \4 g! y
frequency of cell-cycle-associated markers can be used; I, R0 i3 X% `/ v" m3 s* Z
for the differential diagnosis of malignant and benign DC tumours.8 I5 a+ H# Q# s. T* K) e( _1 b0 }
5. [2010 Research]Gut inflammation provides a respiratory electron acceptor for Salmonella
) e9 `( k: w, ~/ u% L  ?Sebastian E. Winter1, Parameth Thiennimitr1,2, Maria G. Winter1, Brian P. Butler1, Douglas L. Huseby3, Robert W. Crawford1,  z- o1 d* x8 b/ G' F( K7 S% b
Joseph M. Russell1, Charles L. Bevins1, L. Garry Adams4, Rene′e M. Tsolis1, John R. Roth3 & Andreas J. Ba¨umler12 ^, c2 i; p  d+ ~) m5 B
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Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence  k% |' }7 l- W7 D# j# q% C8 R
factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response, Y) D, _& g* \
enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through" a. d8 o8 K( r. x/ R
unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with" M! l! ^6 Q/ L0 d, {; i
endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate.5 D7 l6 @+ z  R, J3 `
The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S.
# L5 |( V0 ]  hTyphimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium
( D( s+ N8 j2 u0 ^1 m+ [* S- Wvirulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use, u9 s* p" Y7 p; W" d( e
respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for
0 d" i0 @/ w* @) o0 `5 N6 O5 l5 ithe biology of this diarrhoeal pathogen.
3 u4 P% S; T' ]. j( y6. [2010 Research]Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels- [; l- E3 O  E: P9 w- d6 ?
Bertrand Coste,1 Jayanti Mathur,2 Manuela Schmidt,1 Taryn J. Earley,1 Sanjeev Ranade,1
; O6 d; @& d8 N3 e/ V6 S$ V) U3 CMatt J. Petrus,2 Adrienne E. Dubin,1 Ardem Patapoutian1,2*9 ~) h$ S# l# f3 l- n! N, H9 Z* ~

3 _2 m& L' {; W# L3 CMechanical stimuli drive many physiological processes, including touch and pain sensation,
- n9 d& e% a" o) x, ^  whearing, and blood pressure regulation. Mechanically activated (MA) cation channel activities
3 |9 o6 D% |( n1 f0 Yhave been recorded in many cells, but the responsible molecules have not been identified.' L% P" d8 }- j' t
We characterized a rapidly adapting MA current in a mouse neuroblastoma cell line. Expression
$ G8 D3 t; Q" p! w+ _' W. ^, Z7 i- ]profiling and RNA interference knockdown of candidate genes identified Piezo1 (Fam38A) to be
' d- O* @* O8 P, [7 z8 Z0 w( f$ R$ S0 @required for MA currents in these cells. Piezo1 and related Piezo2 (Fam38B) are vertebrate
: F( m& C0 S* ~$ wmultipass transmembrane proteins with homologs in invertebrates, plants, and protozoa.
0 K% d1 }6 N0 {( E  q/ s9 ^Overexpression of mouse Piezo1 or Piezo2 induced two kinetically distinct MA currents. Piezos
% t) L5 m0 U& ~1 Y1 pare expressed in several tissues, and knockdown of Piezo2 in dorsal root ganglia neurons
9 B* `4 z8 R! x1 dspecifically reduced rapidly adapting MA currents. We propose that Piezos are components of
. @5 j% `# l" f2 {8 B4 B2 z+ OMA cation channels.7 R  f+ I0 _; ?* n7 K
7. [2010 Research]Platelets Amplify Inflammation in Arthritis via Collagen-Dependent Microparticle Production
8 A, Q; R$ S8 [7 F! wEric Boilard,1 Peter A. Nigrovic,1,2 Katherine Larabee,1 Gerald F. M. Watts,1
! T0 Z# W% Q' vJonathan S. Coblyn,1 Michael E. Weinblatt,1 Elena M. Massarotti,1+ C1 Q( p6 H  F: `) c# W4 `
Eileen Remold-O’Donnell,3 Richard W. Farndale,4 Jerry Ware,5 David M. Lee1*4 L6 i5 b. y$ _6 R: k4 s7 U
- {+ i! E3 ?' n: Y9 s2 }
In addition to their pivotal role in thrombosis and wound repair, platelets participate in1 y( \# W( D) }
inflammatory responses. We investigated the role of platelets in the autoimmune disease/ K/ n* d: Z9 {; V5 w
rheumatoid arthritis. We identified platelet microparticles—submicrometer vesicles elaborated by
$ d# M, _( s0 {/ p5 C& Y5 c3 |activated platelets—in joint fluid from patients with rheumatoid arthritis and other forms of
9 |8 d" b3 G4 _4 o, hinflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet' U* L+ y3 J/ S# j# h
microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via
5 ]/ ~) }4 S- g% a0 `% Zinterleukin-1. Consistent with these findings, depletion of platelets attenuated murine
& r0 l8 j  o# s! Vinflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the1 D' W9 n& Y2 q+ U
collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis
1 k* l, o, [4 ^pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets' P! ~( _, Y& f  J
and their activation-induced microparticles in inflammatory joint diseases.: w8 ]  I) _8 i7 J, P7 e) h1 a! m* b
8. [2010 Research]The architecture of respiratory complex I
4 A8 K$ r( y) \, KRouslan G. Efremov*, Rozbeh Baradaran* & Leonid A. Sazanov7 u  q* H$ a9 Y& W
9 w! R7 `$ d2 O' B- G) G; l
Complex I is the first enzyme of the respiratory chain and has a central role in cellular energy production, coupling electron
+ X$ U# J! J$ ?( a, h4 ^transfer between NADH and quinone to proton translocation by an unknown mechanism. Dysfunction of complex I has been
6 v+ G9 ?; s$ Dimplicated in many human neurodegenerative diseases. We have determined the structure of its hydrophilic domain
9 c+ `+ M/ w. K# q3 fpreviously. Here, we report the a-helical structure of the membrane domain of complex I from Escherichia coli at 3.9A°# w0 J! Q" Z- E- l
resolution. The antiporter-like subunits NuoL/M/Neach contain 14 conserved transmembrane (TM) helices. Two of them are% V) R* ^/ z$ {
discontinuous, as in some transporters. Unexpectedly, subunit NuoL also contains a 110-A° long amphipathic a-helix, spanning% t  L% K8 T9 p3 {4 P
almost the entire length of the domain. Furthermore, we have determined the structure of the entire complex I from Thermus" r/ C& l1 L" R
thermophilus at 4.5A°# M' @3 Z- M8 y; i$ h# m
resolution. The L-shaped assembly consists of the a-helicalmodel for themembrane domain, with 63TM1 z! H: g5 a; ~& S8 r$ _" _6 V( f- J
helices, and the known structure of the hydrophilic domain. The architecture of the complex provides strong clues about the
2 T( k& T2 Y6 y8 s- @3 G# I, O, `coupling mechanism: the conformational changes at the interface of the two main domains may drive the long amphipathic
7 y3 z; s! J; t5 `  n: z, ~& ~4 x0 ~a-helix of NuoL in a piston-like motion, tilting nearby discontinuous TM helices, resulting in proton translocation.
: ?- s/ U1 {8 |' Y# `9 `, Z, e[hide][/hide]

军医

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ivantanqi

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