2010 Some Hot Research & Report Papers

清风闲云

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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。+ R: R8 S  d7 q  Z: v
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。
1 w7 T" e- k4 M& W0 A0 s目录：
; ~% Q8 C4 E0 G! A3 v& W1.[2010 Research]A Septin Diffusion Barrier at the Base of the Primary Cilium Maintains Ciliary Membrane Protein Distribution
' H2 H. K, D  K, @8 {Qicong Hu,1 Ljiljana Milenkovic,2,3 Hua Jin,4 Matthew P. Scott,2,3,5–8
9 `' w3 {& E) G" M/ T: aMaxence V. Nachury,4 Elias T. Spiliotis,9* W. James Nelson1,4*# A: f/ R4 S1 Y+ K. Z& U# P
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In animal cells, the primary cilium transduces extracellular signals through signaling receptors
# R9 |$ M- v4 B7 X3 V" o1 _localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the. \' _& s) L4 W9 k
cilium is unknown. We found that ciliary membrane proteins were highly mobile, but their
; D6 i: L( m6 g! e' g6 ?diffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member* t/ T, o$ T3 }  c! r/ d
of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast,2 r/ X6 s: u* s& N4 E& d; h; I  D7 R
localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane
. G& j7 L2 q- ]" Iprotein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus,* G- `! s+ B8 A- e( }2 q# R9 |; e
SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for7 o, B/ [1 n1 R. E5 P  n3 ?
retaining receptor-signaling pathways in the primary cilium.
- w9 s' Y7 _( C- l2 L  j- ~7 z2. [2010 Research]Cancer Statistics5 y4 R# R, e! g: ?
3. [2010 Research]Dendritic Cells in Systemic Lupus Erythematosus
; X- ]- A, G- c. AHeather M. Seitz
  O! n6 ?3 i1 L2 m. }Johnson County Community College, Science Division, Overland Park,( [* Z% ?# s' b
Kansas, USA
( x' Z& \+ h: T) N- X! ZGlenn K. Matsushima
! h5 h! ^6 r9 T7 Q9 p6 q9 M5 N3 SUNC Neuroscience Center, Department of Microbiology & Immunology,
2 p  s4 ?1 }* Z4 a$ F* _/ c$ }Program for Molecular Biology & Biotechnology, University of North
+ x' }+ N; h& f% \( fCarolina at Chapel Hill, Chapel Hill, North Carolina, USA& K7 K: h. K# L, H! L1 z
2 j, F# K$ V( Z! V: E' l5 E3 S- X
Systemic lupus erythematosus (SLE) persists as a chronic inflammatory autoimmune; K) |- U" a( a/ N  G0 M, s. ]
disease and is characterized by the production of autoantibodies
2 y! \% ?3 Q/ @and immune complexes that affect multiple organs. The underlying mechanism1 R* D1 q8 @! o7 V3 S% m
that triggers and sustains disease are complex and involve certain
  P8 X  O$ l- J* w  d1 R8 asusceptibility genes and environmental factors. There have been several immune
+ }" a# J( T: d. ?4 C& omediators linked to SLE including cytokines and chemokines that have. t# Y3 }( x! w  c9 o( a5 g
been reviewed elsewhere [1–3]. A number of articles have reviewed the role& G9 q% g2 w' f: P
of B cells and T cells in SLE [4–10]. Here, we focus on the role of dendritic
  Y+ }9 U+ X/ [+ Q$ Xcells (DC) and innate immune factors that may regulate autoreactive B cells.
  K* x- J& i- h; f" R& U/ M4. [2010 Research]Differential immunophenotypic analysis of dendritic cell tumours
) I$ w6 V2 B9 _9 YTomohiko Orii,1,2 Hiroaki Takeda,2 Sumio Kawata,2 Kunihiko Maeda,1
( I# Q! q" a- k+ q! Z4 pMitsunori Yamakawa1  M  p/ y% h" J# J+ u3 w5 a% J' s
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ABSTRACT$ D8 I2 D2 L' g  j3 a; `
Aims The phenotypic and biological characteristics of+ j* i8 ^+ U( d- ^( }/ h, Q
dendritic cell (DC) tumours have not been fully9 @# J8 p2 G6 q. W, O* J! X
elucidated. The aim of this study was to compare the' r) J7 y0 }9 u( N5 u
immunophenotypic characteristics of DC-related markers
5 \+ D& |  {' ^7 k. b' ?' ~and cell-cycle-associated markers among DC tumours
/ G# D  n; `( |  S6 x' Sand finally to utilise them for differential diagnosis of DC
' A( Z0 @4 g+ m2 o0 m' O, Vtumours.# a1 O: h0 |6 @5 T
Methods Tissue sections from 28 patients with DC, Z+ s! L* M1 \- ^( f. ?  |
tumours were immunohistochemically examined using
" l% _' a  i% L+ LDC-related and cell-cycle-associated markers.
; R1 J* r" ~, Q5 PResults The Langerhans cell histiocytosis (LCH) and; n" o: l# l0 O1 f
Langerhans cell sarcoma (LCS) samples were positive for
6 e* f4 u. Y/ K$ rS-100 protein, CD1a, Langerin, fascin, DEC-205 and DCSIGN.
" o% w7 S9 \1 `Interdigitating dendritic cell sarcoma (IDCS) was4 i# {6 ~7 |: Q
positive for S-100 protein and fascin and negative for( q; U- O8 S6 [  D3 u2 C! \4 C
Langerin. In addition, two IDCS samples were positive for. G% D/ T3 `3 X* `
CD1a, DEC-205 and DC-SIGN. The labelling indices of9 E( M: i. r6 w9 D7 u# ?
Ki-67, cyclin A, cyclin B1 and acetylated histone H3 on the
/ ?# I) N* y1 e: V* ^7 S) {' gLCS and IDCS specimens were significantly higher than
- T4 E% Q: Z1 }+ v/ u, Kthose on the LCH specimens. The expression of p53 was2 y. N: j1 `5 w. K
also significantly higher in the LCS specimens than in the4 W0 M% ?+ ?* D; M- w, J/ e' W
LCH specimens. The numbers of infiltrating CD123+ and3 [4 Y4 `( l( r$ m( }0 n) h
FOXP3+ cells were also significantly higher in the LCS$ [3 N/ B. ?1 T, Z+ G5 r1 F
samples than in the LCH and IDCS samples. Follicular
6 U/ C9 {1 b4 h9 `' x! a$ G: {% G, Udendritic cell sarcoma was distinguished from other DC9 [; o& V* o: P0 ^9 l& d2 O$ }
tumours by the lack of DC-SIGN, Langerin and DCE-205.- l: o, b4 E1 T1 ]" x, @$ Y; d" {
Conclusions These results suggest that Langerin can be; J5 F, w, V1 a5 e, d$ L; B
used to distinguish LCS from IDCS, and DC-SIGN and
: U2 w( _# c9 R1 GDEC-205 can be used to identify DC tumour cells. The- C' ~4 s0 y9 d. ^
frequency of cell-cycle-associated markers can be used
7 c# H, A0 L* X" z6 Ofor the differential diagnosis of malignant and benign DC tumours.
; P- s% G% j- T' [5. [2010 Research]Gut inflammation provides a respiratory electron acceptor for Salmonella
* J. y( `4 e8 A. C* N  _! ~: l  p5 ~Sebastian E. Winter1, Parameth Thiennimitr1,2, Maria G. Winter1, Brian P. Butler1, Douglas L. Huseby3, Robert W. Crawford1,- P" }, Z8 I% c' b
Joseph M. Russell1, Charles L. Bevins1, L. Garry Adams4, Rene′e M. Tsolis1, John R. Roth3 & Andreas J. Ba¨umler1
6 t" g# X/ b& I2 `/ N( U+ @" s
3 D, E- _( J8 m, @2 nSalmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence' S, `5 J/ m: u8 \. y/ @- T$ ~; Y, |
factors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response. a/ q% ?6 P& L, \4 B2 k0 N7 @" _' E3 p
enhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through
8 H& s* W0 S4 ^( G% f2 punknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with! m) F1 L# F! L5 }* f
endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate.
% B' p3 O8 R& L7 r8 z& H! y0 wThe genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S.# \8 D! y1 y0 I6 J% W! {3 Z
Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium
- v+ K2 r7 i0 R  h+ v( ivirulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use
9 O" m5 t# R1 W) m; @respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for
+ J6 ^+ q/ Z% r3 F# Tthe biology of this diarrhoeal pathogen.2 W: X& ~9 r! }1 a3 S
6. [2010 Research]Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels9 n3 n4 }+ O+ S2 G% F$ p
Bertrand Coste,1 Jayanti Mathur,2 Manuela Schmidt,1 Taryn J. Earley,1 Sanjeev Ranade,1" k8 [# Z+ Q% x( g/ ~3 U7 b
Matt J. Petrus,2 Adrienne E. Dubin,1 Ardem Patapoutian1,2*5 z# G; d9 ]/ T4 d2 r4 C
" {6 Q9 f8 B8 y8 u
Mechanical stimuli drive many physiological processes, including touch and pain sensation,
& t! r& N( Y, {0 Nhearing, and blood pressure regulation. Mechanically activated (MA) cation channel activities2 L5 ^1 G# u, f. |8 W1 V
have been recorded in many cells, but the responsible molecules have not been identified.
( P( S6 N! D' U+ F3 mWe characterized a rapidly adapting MA current in a mouse neuroblastoma cell line. Expression7 J2 Z& u, ~% f# d4 B! ^
profiling and RNA interference knockdown of candidate genes identified Piezo1 (Fam38A) to be8 q3 D. N1 ]/ z" U0 P; x- z5 S
required for MA currents in these cells. Piezo1 and related Piezo2 (Fam38B) are vertebrate1 I. L. b* t+ H: n" ]/ I
multipass transmembrane proteins with homologs in invertebrates, plants, and protozoa.
: v9 X! ]3 }6 m2 Y+ DOverexpression of mouse Piezo1 or Piezo2 induced two kinetically distinct MA currents. Piezos
! v7 H# c6 e2 D, dare expressed in several tissues, and knockdown of Piezo2 in dorsal root ganglia neurons
! ]# Z/ T- J4 e4 Cspecifically reduced rapidly adapting MA currents. We propose that Piezos are components of
& Y3 }2 H* D2 F* Q, m; O& RMA cation channels.
+ P4 d/ b: D& R) I5 d2 x7. [2010 Research]Platelets Amplify Inflammation in Arthritis via Collagen-Dependent Microparticle Production
- \" e) w5 Q* I% S2 J1 PEric Boilard,1 Peter A. Nigrovic,1,2 Katherine Larabee,1 Gerald F. M. Watts,1
& C0 u5 r  }/ V4 h) X% D2 O- A( |Jonathan S. Coblyn,1 Michael E. Weinblatt,1 Elena M. Massarotti,1; F9 ~" I2 @) C1 I3 Z
Eileen Remold-O’Donnell,3 Richard W. Farndale,4 Jerry Ware,5 David M. Lee1*
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In addition to their pivotal role in thrombosis and wound repair, platelets participate in* X" ~4 D6 R- V; {) k
inflammatory responses. We investigated the role of platelets in the autoimmune disease
7 r8 Y0 v$ b  q9 z" prheumatoid arthritis. We identified platelet microparticles—submicrometer vesicles elaborated by
7 w( a/ B4 d" Z; Factivated platelets—in joint fluid from patients with rheumatoid arthritis and other forms of+ q4 Z5 _9 k$ |' D( m
inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet( w0 K" V( D8 G* k
microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via
- l0 U9 s8 t- j3 ^; n7 einterleukin-1. Consistent with these findings, depletion of platelets attenuated murine
& v: _# e) c  ~: |$ Rinflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the& `. G" U+ P) j% j6 g: l- ?# }
collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis& p  N, ~+ y* A
pathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets
+ X* P1 _& n8 E, F) ~and their activation-induced microparticles in inflammatory joint diseases.1 P, q7 F' X  ?/ j( R' F
8. [2010 Research]The architecture of respiratory complex I
+ v( {- ^4 K$ |$ _Rouslan G. Efremov*, Rozbeh Baradaran* & Leonid A. Sazanov3 |7 ~% ^3 a+ r0 z
* a7 M- X, X4 }5 G3 f6 e& A
Complex I is the first enzyme of the respiratory chain and has a central role in cellular energy production, coupling electron/ Z. h; ?7 n" o& V/ A. S
transfer between NADH and quinone to proton translocation by an unknown mechanism. Dysfunction of complex I has been+ h7 R8 b3 E% s, _, Q) }7 d
implicated in many human neurodegenerative diseases. We have determined the structure of its hydrophilic domain; j* j5 ?9 B$ p
previously. Here, we report the a-helical structure of the membrane domain of complex I from Escherichia coli at 3.9A°. O* v) {  \9 k9 a' I
resolution. The antiporter-like subunits NuoL/M/Neach contain 14 conserved transmembrane (TM) helices. Two of them are' _9 [$ T. p% E
discontinuous, as in some transporters. Unexpectedly, subunit NuoL also contains a 110-A° long amphipathic a-helix, spanning; c/ q( N7 z/ j( D3 u
almost the entire length of the domain. Furthermore, we have determined the structure of the entire complex I from Thermus
" o2 j0 U5 b2 }thermophilus at 4.5A°. M: \6 D( b/ U4 X+ z
resolution. The L-shaped assembly consists of the a-helicalmodel for themembrane domain, with 63TM
7 q1 P% s) h1 H& A( W1 V) whelices, and the known structure of the hydrophilic domain. The architecture of the complex provides strong clues about the. E( X2 M/ z: N. |
coupling mechanism: the conformational changes at the interface of the two main domains may drive the long amphipathic
3 R- V! @! k9 ~$ w5 A; U( na-helix of NuoL in a piston-like motion, tilting nearby discontinuous TM helices, resulting in proton translocation., _4 A% ^. }9 s: m
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军医

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军医

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ivantanqi

Thanks for sharing

lifescience1

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sky蓝

老大,我好崇拜你哟  

大小年

彪悍的人生不需要解释。  

bluesuns

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beautylive

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laoli1999

一个子 没看懂