2010 Some Hot Research & Report Papers

清风闲云

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" X, N( a6 q2 G8 t" I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。$ u9 [, a" r, l; Y, c
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。
) I3 F, x6 J: {5 |6 B: y9 M目录：# h" H" P4 z0 ^; N+ L+ f: a4 l
1.[2010 Research]A Septin Diffusion Barrier at the Base of the Primary Cilium Maintains Ciliary Membrane Protein Distribution
. R- O+ r% {7 a! G3 i) |! yQicong Hu,1 Ljiljana Milenkovic,2,3 Hua Jin,4 Matthew P. Scott,2,3,5–8- r! l: U6 d/ y* B# v9 h
Maxence V. Nachury,4 Elias T. Spiliotis,9* W. James Nelson1,4*" ~3 h7 S( L( s  J, v

5 d- g, ^+ U: W( O& jIn animal cells, the primary cilium transduces extracellular signals through signaling receptors7 v( G8 O  @6 N. S4 t1 g0 z0 D
localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the
2 `2 Z8 {# C3 p  q: Ccilium is unknown. We found that ciliary membrane proteins were highly mobile, but their
; @0 i0 b" {5 Z+ r- \, \diffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member6 \* M6 Y# O) C* d6 j# x
of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast,
3 E* }. B: \: |" x4 {  N! _: r! t3 glocalized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane
* Y) Z# J* z' l2 H+ T& \protein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus,
) k# k' L5 c# w; NSEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for
/ H+ z) L1 N3 G, x) L9 Lretaining receptor-signaling pathways in the primary cilium.+ t4 L2 o) b7 }. b
2. [2010 Research]Cancer Statistics
& B4 Z; P9 H+ j- t3. [2010 Research]Dendritic Cells in Systemic Lupus Erythematosus* O0 V  k) q9 G& l7 _3 J0 t
Heather M. Seitz
1 @/ P; S6 H1 }" hJohnson County Community College, Science Division, Overland Park,
; d& }+ n- O( LKansas, USA
, T8 K4 }8 }+ r0 B& H0 w6 J! c1 zGlenn K. Matsushima
4 |' Y" g9 R; M) `9 [UNC Neuroscience Center, Department of Microbiology & Immunology,
* ^* C5 u- Z/ B7 @" w- @" VProgram for Molecular Biology & Biotechnology, University of North( O& P7 E" b1 W  v. n0 s7 ^+ Z/ f
Carolina at Chapel Hill, Chapel Hill, North Carolina, USA9 y. {5 e) S* `8 Y

( H( N: }/ z: b" U0 B6 G* r) PSystemic lupus erythematosus (SLE) persists as a chronic inflammatory autoimmune* [" Z1 q4 V0 \5 V; g, ]
disease and is characterized by the production of autoantibodies
) t5 U0 e+ ~6 y/ W2 _7 rand immune complexes that affect multiple organs. The underlying mechanism
5 Q" t! q& Y0 v' L+ L' Mthat triggers and sustains disease are complex and involve certain
( m, {# T9 e; \% Psusceptibility genes and environmental factors. There have been several immune7 E& v# z  m8 u) T: M1 P) Y1 _
mediators linked to SLE including cytokines and chemokines that have" N6 x1 M! B+ Y* `1 A# H
been reviewed elsewhere [1–3]. A number of articles have reviewed the role1 |! H0 O9 e, `; O) z
of B cells and T cells in SLE [4–10]. Here, we focus on the role of dendritic
3 m" V3 x; H4 J5 E7 G# R- xcells (DC) and innate immune factors that may regulate autoreactive B cells.. c0 ^( e6 s9 y" ^6 c
4. [2010 Research]Differential immunophenotypic analysis of dendritic cell tumours
; y: O: Q0 m  m( t/ BTomohiko Orii,1,2 Hiroaki Takeda,2 Sumio Kawata,2 Kunihiko Maeda,1
( L6 N/ D$ N9 m, HMitsunori Yamakawa1
! q* n& d2 Z/ G' z2 N
8 a1 N0 _. m7 O! oABSTRACT4 U/ \: I9 T4 c" I0 Q: {: H
Aims The phenotypic and biological characteristics of" e6 Q$ d7 H: A1 e: S& [* o; U
dendritic cell (DC) tumours have not been fully& B1 n# Z3 W/ @+ t% }
elucidated. The aim of this study was to compare the
0 g# ~% e" Y: |2 x+ l" ]% v1 @& mimmunophenotypic characteristics of DC-related markers
% M1 Z$ A5 R4 C0 wand cell-cycle-associated markers among DC tumours! h& h& h3 g/ `$ y, r
and finally to utilise them for differential diagnosis of DC
" T: K) J3 o& Qtumours.
  Q0 _2 a/ g! q' eMethods Tissue sections from 28 patients with DC
. _% I- o9 Y$ Z' u; ~, d  l) c7 Ytumours were immunohistochemically examined using
& Y9 [7 j; K; D& p6 o2 \DC-related and cell-cycle-associated markers.9 J7 \+ B8 ^9 B7 {: H1 B5 X
Results The Langerhans cell histiocytosis (LCH) and# k+ w4 _, z% _2 C
Langerhans cell sarcoma (LCS) samples were positive for. M6 w# y& G8 _6 K2 n
S-100 protein, CD1a, Langerin, fascin, DEC-205 and DCSIGN.) v0 v( X. o) R& j  |  F% [. o% w
Interdigitating dendritic cell sarcoma (IDCS) was& g5 d$ }" ~) ]5 H
positive for S-100 protein and fascin and negative for
1 Q4 Q) V) L2 p) ]4 ^( mLangerin. In addition, two IDCS samples were positive for
$ @& W/ m6 ]- X/ c% wCD1a, DEC-205 and DC-SIGN. The labelling indices of. ~! x4 Q0 [! [9 ]; ]- y
Ki-67, cyclin A, cyclin B1 and acetylated histone H3 on the
' L# |+ D! ^. x, i3 D2 M: lLCS and IDCS specimens were significantly higher than) |" D0 O3 N4 U- E: Q/ H7 z( [
those on the LCH specimens. The expression of p53 was
' X; d: q! R( @# }6 g% n( y. q- halso significantly higher in the LCS specimens than in the8 u* z' f5 ~% h3 M* k
LCH specimens. The numbers of infiltrating CD123+ and8 g! v+ z) q8 E/ J5 L0 J
FOXP3+ cells were also significantly higher in the LCS
% Y5 i7 i) Y+ i7 Q6 _! Fsamples than in the LCH and IDCS samples. Follicular
' m6 V! O5 L7 v" _* ldendritic cell sarcoma was distinguished from other DC7 }3 [8 ~0 ]4 N1 Q" l
tumours by the lack of DC-SIGN, Langerin and DCE-205.. S" }! T# n4 q- {
Conclusions These results suggest that Langerin can be
: n+ R# Y' V( Dused to distinguish LCS from IDCS, and DC-SIGN and2 {9 w$ F& V) o& o
DEC-205 can be used to identify DC tumour cells. The
: Y) J$ P( F+ k- M; x( m: l/ ]frequency of cell-cycle-associated markers can be used
$ D, M" R( i+ t, G) s& \for the differential diagnosis of malignant and benign DC tumours.- |/ {% p2 U2 J5 h% c
5. [2010 Research]Gut inflammation provides a respiratory electron acceptor for Salmonella* t* f, z4 S8 j
Sebastian E. Winter1, Parameth Thiennimitr1,2, Maria G. Winter1, Brian P. Butler1, Douglas L. Huseby3, Robert W. Crawford1,! l0 Z- I- A8 c
Joseph M. Russell1, Charles L. Bevins1, L. Garry Adams4, Rene′e M. Tsolis1, John R. Roth3 & Andreas J. Ba¨umler1
0 w0 U% K0 ^" f4 d1 q# }- x$ S8 n1 v3 n
Salmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence
, X3 ^9 u  f) d' zfactors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response
3 j; _. n8 x* Jenhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through
/ K$ b5 s: A/ v* w% Funknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with; e/ y+ Q5 O& @% h
endogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate., ~+ Z/ c! Z! j5 f2 j4 ]" L  ]
The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S.  V3 M$ a9 X, i  a0 j
Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium% v2 V5 F/ i+ h# p, X
virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use$ S' I; N- j. j, k" V" j) z
respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for* X6 I5 {5 [" q
the biology of this diarrhoeal pathogen.% Y& H/ [7 W% X! G+ Z1 [
6. [2010 Research]Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels/ Z" ]+ F4 O( ?9 q) Q; ]
Bertrand Coste,1 Jayanti Mathur,2 Manuela Schmidt,1 Taryn J. Earley,1 Sanjeev Ranade,1
+ P; K2 Q9 d# i! ~# Z; m7 {- d) T- xMatt J. Petrus,2 Adrienne E. Dubin,1 Ardem Patapoutian1,2*
1 i2 u& a5 Z7 n- V" H8 |3 I! p5 ?
Mechanical stimuli drive many physiological processes, including touch and pain sensation,
9 d$ e4 s9 j8 P0 Whearing, and blood pressure regulation. Mechanically activated (MA) cation channel activities* d% S# L; C* S
have been recorded in many cells, but the responsible molecules have not been identified.
  X% A8 D# M8 x2 [" \& AWe characterized a rapidly adapting MA current in a mouse neuroblastoma cell line. Expression
% l0 c  {9 {/ Z/ R0 rprofiling and RNA interference knockdown of candidate genes identified Piezo1 (Fam38A) to be2 Q! j- r" b/ M: F# H$ U% I
required for MA currents in these cells. Piezo1 and related Piezo2 (Fam38B) are vertebrate
9 y; b* S3 [) {3 F0 W' A! s+ imultipass transmembrane proteins with homologs in invertebrates, plants, and protozoa.
9 X9 m+ e( `* L  Y5 bOverexpression of mouse Piezo1 or Piezo2 induced two kinetically distinct MA currents. Piezos
( e: u, W' T4 E, E8 mare expressed in several tissues, and knockdown of Piezo2 in dorsal root ganglia neurons  {" x! k; l" e/ s2 @
specifically reduced rapidly adapting MA currents. We propose that Piezos are components of6 s3 p) \+ c3 r: _# s% L4 a6 n
MA cation channels.' M) R- m- O9 k3 g/ P
7. [2010 Research]Platelets Amplify Inflammation in Arthritis via Collagen-Dependent Microparticle Production
: W4 Z" U) [. Z6 {" NEric Boilard,1 Peter A. Nigrovic,1,2 Katherine Larabee,1 Gerald F. M. Watts,1
& x  E% [: ?, L% NJonathan S. Coblyn,1 Michael E. Weinblatt,1 Elena M. Massarotti,1  p) ~. U6 o- G6 o/ N* _$ v' `
Eileen Remold-O’Donnell,3 Richard W. Farndale,4 Jerry Ware,5 David M. Lee1*" `- K& D* r; W: H1 s

+ y5 T; p$ L, Y8 Z3 z# q& D7 lIn addition to their pivotal role in thrombosis and wound repair, platelets participate in' s' f9 T0 A. [8 R( n' z( W' ~. E
inflammatory responses. We investigated the role of platelets in the autoimmune disease* B& k+ p. d, I# P9 b! }
rheumatoid arthritis. We identified platelet microparticles—submicrometer vesicles elaborated by
! D2 C! R+ l. D& \# r( Z6 kactivated platelets—in joint fluid from patients with rheumatoid arthritis and other forms of
* }7 `6 S, ~( Z' _+ finflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet* v$ D* V+ K' r. M$ O
microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via6 P, A% K5 s! Z9 ?+ Z
interleukin-1. Consistent with these findings, depletion of platelets attenuated murine
3 `8 j. `$ a7 V4 Oinflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the( O0 A3 [: x% u: p' a
collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis
1 }5 }: X5 F6 R% @3 Hpathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets1 I6 G0 K# w( s" J' T4 ~2 S# L
and their activation-induced microparticles in inflammatory joint diseases.
! j1 q& d$ U8 x. _8. [2010 Research]The architecture of respiratory complex I0 U5 m+ R& S" s: e9 R% O" p
Rouslan G. Efremov*, Rozbeh Baradaran* & Leonid A. Sazanov, _0 X+ ^# J& F

/ z/ {: e% g; p2 @# AComplex I is the first enzyme of the respiratory chain and has a central role in cellular energy production, coupling electron" n2 a' c; U# R6 W$ [
transfer between NADH and quinone to proton translocation by an unknown mechanism. Dysfunction of complex I has been
$ c) V" K5 ?& U( S& e: h( Eimplicated in many human neurodegenerative diseases. We have determined the structure of its hydrophilic domain  O3 c* k5 v2 _4 T, N0 C
previously. Here, we report the a-helical structure of the membrane domain of complex I from Escherichia coli at 3.9A°; i+ L& }1 B0 Y
resolution. The antiporter-like subunits NuoL/M/Neach contain 14 conserved transmembrane (TM) helices. Two of them are
8 H8 L3 N4 G" m! ydiscontinuous, as in some transporters. Unexpectedly, subunit NuoL also contains a 110-A° long amphipathic a-helix, spanning9 K' K+ T* R% O
almost the entire length of the domain. Furthermore, we have determined the structure of the entire complex I from Thermus. p9 j( T& V$ w7 ^4 S$ p; i
thermophilus at 4.5A°: T2 v5 M$ t4 J: D: h
resolution. The L-shaped assembly consists of the a-helicalmodel for themembrane domain, with 63TM
  B  L/ {2 |4 p6 P( c; Qhelices, and the known structure of the hydrophilic domain. The architecture of the complex provides strong clues about the
( N* C9 x; }+ b- a' g4 U0 S7 acoupling mechanism: the conformational changes at the interface of the two main domains may drive the long amphipathic
$ F4 E) e6 E6 o2 Z' Na-helix of NuoL in a piston-like motion, tilting nearby discontinuous TM helices, resulting in proton translocation.
, r2 D! I5 z& [. b, Z- `% {4 l( M" P[hide][/hide]

军医

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ivantanqi

Thanks for sharing

lifescience1

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sky蓝

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大小年

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laoli1999

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