标题: 2010 Some Hot Research & Report Papers [打印本页] 作者: 清风闲云 时间: 2011-5-5 23:53 标题: 2010 Some Hot Research & Report Papers
本帖最后由 细胞海洋 于 2011-5-6 00:17 编辑 ! r% n" a" Z5 }$ j* `; ^- X2 ~) X; m7 I4 E# \
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。9 y9 R! p& T; U0 ~% X& Q+ j. ?/ |' S7 m
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。 + m+ U/ u: J1 }! Z2 H目录：! M) H% i7 }' R) L
1.[2010 Research]A Septin Diffusion Barrier at the Base of the Primary Cilium Maintains Ciliary Membrane Protein Distribution ! ]! [3 V5 z Z5 W/ q# u! iQicong Hu,1 Ljiljana Milenkovic,2,3 Hua Jin,4 Matthew P. Scott,2,3,5–8 & ^7 K* ]" T4 G" @Maxence V. Nachury,4 Elias T. Spiliotis,9* W. James Nelson1,4* / d* G5 B- O, U4 J8 J# R. n6 ~: e7 X; c9 {9 @" O( i
In animal cells, the primary cilium transduces extracellular signals through signaling receptors% T, z) F, a o; n+ s, i5 X
localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the + ~- z9 ^3 d- u I1 w3 \- Pcilium is unknown. We found that ciliary membrane proteins were highly mobile, but their & X& V2 G4 h4 d; S; W! l2 w1 b& Hdiffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member) R1 n# @: H. U3 g+ y* S
of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast,3 R, K$ A o* V" M
localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane' Q$ ~$ n- J* ^4 I2 L% e, [
protein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus,7 u0 m( i* L9 [% _7 J0 i. p. d
SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for$ q3 z0 f0 Z7 W$ B* w
retaining receptor-signaling pathways in the primary cilium. 0 j! z; I% g% d7 P. e, B: [2. [2010 Research]Cancer Statistics% B9 K! {3 w, g
3. [2010 Research]Dendritic Cells in Systemic Lupus Erythematosus 5 y- c* @- h: C0 q" G( G, aHeather M. Seitz ) y2 k# v: T2 f! I0 U( N' BJohnson County Community College, Science Division, Overland Park, , Y, ?* @- n) d( [1 n0 @Kansas, USA 0 q( S$ m" x+ `Glenn K. Matsushima V& q2 j3 m, A- F
UNC Neuroscience Center, Department of Microbiology & Immunology, & @/ J1 l; Y3 ?: {8 ?+ |Program for Molecular Biology & Biotechnology, University of North0 X9 P3 {+ b, U) E/ K& Y
Carolina at Chapel Hill, Chapel Hill, North Carolina, USA 8 Z: r4 b( G" P* ]+ Q1 F( ?. C
Systemic lupus erythematosus (SLE) persists as a chronic inflammatory autoimmune/ M' g( I; ?2 e
disease and is characterized by the production of autoantibodies# u9 y) _ z5 P% K: V( g. [( h& M
and immune complexes that affect multiple organs. The underlying mechanism H% h9 V! L E* k5 |that triggers and sustains disease are complex and involve certain ( c( q/ C& Q' hsusceptibility genes and environmental factors. There have been several immune3 l2 P x1 c- A( C% B, S
mediators linked to SLE including cytokines and chemokines that have 0 ?3 \7 e; `7 P0 h7 Ibeen reviewed elsewhere [1–3]. A number of articles have reviewed the role 8 }0 W6 [* S+ ^, ]of B cells and T cells in SLE [4–10]. Here, we focus on the role of dendritic% |& e" C( I7 b- l, Y5 I
cells (DC) and innate immune factors that may regulate autoreactive B cells. 6 S4 @0 D$ T; N% e* F$ V4. [2010 Research]Differential immunophenotypic analysis of dendritic cell tumours 4 _/ Z8 `* {) _. F* S& i9 l6 nTomohiko Orii,1,2 Hiroaki Takeda,2 Sumio Kawata,2 Kunihiko Maeda,1 4 T0 U7 ?" I( `/ {7 FMitsunori Yamakawa1+ ^4 T( O! Q- }2 F( L! k
% u( p3 V3 D- P5 wABSTRACT& [$ R- s3 }0 p) K) ^! I- p
Aims The phenotypic and biological characteristics of 7 E& }( Z |/ U: y! @% Z% [; a8 {dendritic cell (DC) tumours have not been fully. a9 ?8 c J' p7 p0 ^. U$ x$ u
elucidated. The aim of this study was to compare the! \8 L: ^+ w: f/ K' N2 r
immunophenotypic characteristics of DC-related markers 0 d7 p2 f* Y- Gand cell-cycle-associated markers among DC tumours$ x4 U6 n4 d9 K* n
and finally to utilise them for differential diagnosis of DC 1 T5 L& F# J8 m' S) H" T! Ltumours. ! t3 M6 N! x- p. ]: C4 f9 K8 kMethods Tissue sections from 28 patients with DC 4 s" W9 q: {0 }& w! f2 q) A btumours were immunohistochemically examined using + ^4 v7 n0 V7 P% i; H, V9 NDC-related and cell-cycle-associated markers." M# }; m) E5 z3 h, F
Results The Langerhans cell histiocytosis (LCH) and$ @, H+ r: C, I6 U2 _
Langerhans cell sarcoma (LCS) samples were positive for 2 \7 R" f6 ^6 \S-100 protein, CD1a, Langerin, fascin, DEC-205 and DCSIGN. 2 Y2 ^& [( S8 v4 l- @ Z6 lInterdigitating dendritic cell sarcoma (IDCS) was 3 [0 O0 \; ~, J" `7 opositive for S-100 protein and fascin and negative for / J3 s$ n% \8 ?% s6 P6 sLangerin. In addition, two IDCS samples were positive for 1 s+ s& j4 L$ r6 h9 V% JCD1a, DEC-205 and DC-SIGN. The labelling indices of- ^/ L8 q+ Y2 q
Ki-67, cyclin A, cyclin B1 and acetylated histone H3 on the : I1 u) {; c: U' @. b4 eLCS and IDCS specimens were significantly higher than4 A6 [+ Y7 F4 ]2 R* q
those on the LCH specimens. The expression of p53 was , F1 O0 V! w5 s6 B1 ealso significantly higher in the LCS specimens than in the + N+ M: }% d0 ^; r4 U& ?# Q4 ILCH specimens. The numbers of infiltrating CD123+ and - u) V) F' Y" J4 a8 g7 T. WFOXP3+ cells were also significantly higher in the LCS t t( M! d- S1 A+ z
samples than in the LCH and IDCS samples. Follicular - s# |6 O# d* fdendritic cell sarcoma was distinguished from other DC# q6 }7 K0 X. R* J
tumours by the lack of DC-SIGN, Langerin and DCE-205.8 Q: H; Z @* P* E3 |
Conclusions These results suggest that Langerin can be/ h" p% x7 y4 Y
used to distinguish LCS from IDCS, and DC-SIGN and ; C* j' e- n9 l. s" [" C' a5 q) LDEC-205 can be used to identify DC tumour cells. The6 J" d# Z; j: {% \, l
frequency of cell-cycle-associated markers can be used ! l7 \3 t( b7 g! N. b0 E3 X4 @for the differential diagnosis of malignant and benign DC tumours. * l; a& G, S% u* Q: u5. [2010 Research]Gut inflammation provides a respiratory electron acceptor for Salmonella1 z& ]. v$ w8 n y* V
Sebastian E. Winter1, Parameth Thiennimitr1,2, Maria G. Winter1, Brian P. Butler1, Douglas L. Huseby3, Robert W. Crawford1, % k; u' m% p' E l# C& ^3 a& R$ pJoseph M. Russell1, Charles L. Bevins1, L. Garry Adams4, Rene′e M. Tsolis1, John R. Roth3 & Andreas J. Ba¨umler1 ) Q9 X' b: N" m# g/ d' x! L7 @' ]% c6 I7 S; U7 ]. J b* R
Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence2 ?6 a2 P# G+ Q* r
factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response2 ~9 M; Y4 q( Y% A& z2 j8 F
enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through : t0 W0 f$ m% _) |unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with ) C6 I2 F6 i3 x3 X( [endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate.- Y. Y' g2 L7 u5 o: p$ U
The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S.; x; o+ s* }% Z" ]3 c5 ]8 c: E
Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium 9 q( d. X# V% S0 I# q9 |# ~virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use# i5 t% V3 k* u% G
respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for & T8 Y8 Y3 F3 G) Cthe biology of this diarrhoeal pathogen.; t* l$ @2 [- E: G* H `! _/ V2 q
6. [2010 Research]Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels " C3 D1 U4 \, |, w8 _3 `8 kBertrand Coste,1 Jayanti Mathur,2 Manuela Schmidt,1 Taryn J. Earley,1 Sanjeev Ranade,10 L# J# j1 T* Z0 X
Matt J. Petrus,2 Adrienne E. Dubin,1 Ardem Patapoutian1,2* . V% ^& m# l& {0 } : e. g: J: {6 |0 N% d1 ^7 c% \Mechanical stimuli drive many physiological processes, including touch and pain sensation,# ~+ p1 L0 [: ~( o7 k( |: z
hearing, and blood pressure regulation. Mechanically activated (MA) cation channel activities |7 ?$ r; c6 ]- h3 @
have been recorded in many cells, but the responsible molecules have not been identified.. {# Q/ E6 J# j! Z6 H0 b1 [) q
We characterized a rapidly adapting MA current in a mouse neuroblastoma cell line. Expression ( t2 t% h+ A( aprofiling and RNA interference knockdown of candidate genes identified Piezo1 (Fam38A) to be ; y: c; z6 A8 Erequired for MA currents in these cells. Piezo1 and related Piezo2 (Fam38B) are vertebrate ' \/ u$ u0 H1 L& Fmultipass transmembrane proteins with homologs in invertebrates, plants, and protozoa. # g6 W( P# R9 O9 n4 MOverexpression of mouse Piezo1 or Piezo2 induced two kinetically distinct MA currents. Piezos0 x$ T/ I, V0 P, K% u6 t6 c: A* L
are expressed in several tissues, and knockdown of Piezo2 in dorsal root ganglia neurons& u& [( O2 Z Z, J/ ^0 t) Y
specifically reduced rapidly adapting MA currents. We propose that Piezos are components of , F/ ~) e" H. R( ^7 yMA cation channels. 7 H8 q9 e3 |: U+ A7. [2010 Research]Platelets Amplify Inflammation in Arthritis via Collagen-Dependent Microparticle Production " I2 T. m4 A, `0 o2 WEric Boilard,1 Peter A. Nigrovic,1,2 Katherine Larabee,1 Gerald F. M. Watts,1 & \: @4 k+ R: H% ?. yJonathan S. Coblyn,1 Michael E. Weinblatt,1 Elena M. Massarotti,1 $ t2 J+ k0 D+ c8 x' I! MEileen Remold-O’Donnell,3 Richard W. Farndale,4 Jerry Ware,5 David M. Lee1* * i$ G* Q9 ~! R% v8 e9 z$ `, X4 d ~& o; V/ t0 [% `& pIn addition to their pivotal role in thrombosis and wound repair, platelets participate in `: A7 N" c {% z3 V1 Ainflammatory responses. We investigated the role of platelets in the autoimmune disease3 v" O# W3 i8 I. A
rheumatoid arthritis. We identified platelet microparticles—submicrometer vesicles elaborated by 6 U! c: Z! y# A0 t* y( S3 vactivated platelets—in joint fluid from patients with rheumatoid arthritis and other forms of) p7 E, i. ?$ f
inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet : y" M' Y7 Q8 s7 Z3 `; umicroparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via / b' B2 t/ z: K! Winterleukin-1. Consistent with these findings, depletion of platelets attenuated murine- Y8 s( a! j+ A2 M) H" D
inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the % G& ?! i+ Z6 N# i) @collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis- A& Y* {, U+ U+ O
pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets& w1 ~) [; A; i: h& W5 \" h
and their activation-induced microparticles in inflammatory joint diseases.; B; T+ \9 m0 ?( n* ?6 Y5 y
8. [2010 Research]The architecture of respiratory complex I; K* H' `5 s# J& P2 B
Rouslan G. Efremov*, Rozbeh Baradaran* & Leonid A. Sazanov7 x, ^+ }2 K0 `3 S1 Z0 A
# e/ ? ?9 E, f
Complex I is the first enzyme of the respiratory chain and has a central role in cellular energy production, coupling electron3 q3 p' u- [$ ~! R! O1 U x4 j
transfer between NADH and quinone to proton translocation by an unknown mechanism. Dysfunction of complex I has been 1 f" j1 o: C$ }" V: o, qimplicated in many human neurodegenerative diseases. We have determined the structure of its hydrophilic domain3 @$ W. I7 n) r# g
previously. Here, we report the a-helical structure of the membrane domain of complex I from Escherichia coli at 3.9A°1 m# K* \7 m8 h t: J$ J6 T% Q# G$ b" _4 X
resolution. The antiporter-like subunits NuoL/M/Neach contain 14 conserved transmembrane (TM) helices. Two of them are9 B2 ]5 @* U6 u+ S
discontinuous, as in some transporters. Unexpectedly, subunit NuoL also contains a 110-A° long amphipathic a-helix, spanning , E1 x8 x3 x E) J H1 Galmost the entire length of the domain. Furthermore, we have determined the structure of the entire complex I from Thermus8 N, f8 Z2 r0 P2 `0 l2 w! q' H" ^
thermophilus at 4.5A°- R/ t! [0 R) A) u2 X
resolution. The L-shaped assembly consists of the a-helicalmodel for themembrane domain, with 63TM 3 G* I" ^# g9 F- a* m( ihelices, and the known structure of the hydrophilic domain. The architecture of the complex provides strong clues about the 3 v: f! h3 g6 h: ~coupling mechanism: the conformational changes at the interface of the two main domains may drive the long amphipathic # a) m: A/ C/ R% E: @3 B8 ta-helix of NuoL in a piston-like motion, tilting nearby discontinuous TM helices, resulting in proton translocation. 6 d o( H; I. `& l" n作者: 军医 时间: 2011-5-6 00:58
看看啊作者: 军医 时间: 2011-5-6 00:58
看看啊作者: ivantanqi 时间: 2011-5-6 02:14
Thanks for sharing作者: lifescience1 时间: 2011-5-6 10:11
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