|
- 积分
- 97
- 威望
- 97
- 包包
- 1308
|
本帖最后由 细胞海洋 于 2011-5-6 00:17 编辑 7 P. ~" l7 N7 F( o2 R! K
* |: F! d5 C! I7 H% _$ \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。4 N; O/ L D& I0 s* ~, @+ y% a
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。
0 T; p9 V j* u& h) X目录：
) |* k5 Z# x+ u6 R2 v1.[2010 Research]A Septin Diffusion Barrier at the Base of the Primary Cilium Maintains Ciliary Membrane Protein Distribution ; c8 q* F7 }; z$ d" e @
Qicong Hu,1 Ljiljana Milenkovic,2,3 Hua Jin,4 Matthew P. Scott,2,3,5–8
: O( C9 _7 C3 i) c3 P+ f/ zMaxence V. Nachury,4 Elias T. Spiliotis,9* W. James Nelson1,4*
+ t: M) f/ ~: o9 |/ V- `& V8 K( Z o% } {9 Y
In animal cells, the primary cilium transduces extracellular signals through signaling receptors1 g% M; t, i% K3 s* D" n
localized in the ciliary membrane, but how these ciliary membrane proteins are retained in the" k Z0 R0 c$ a; U, x
cilium is unknown. We found that ciliary membrane proteins were highly mobile, but their
8 |* ^, a# \. D, M# E% w; Vdiffusion was impeded at the base of the cilium by a diffusion barrier. Septin 2 (SEPT2), a member( d! D3 ~- q, q9 i" v4 N
of the septin family of guanosine triphosphatases that form a diffusion barrier in budding yeast,# \' O' m# C$ `! a) i
localized at the base of the ciliary membrane. SEPT2 depletion resulted in loss of ciliary membrane8 c) S( X1 x5 m- O3 q6 M2 A2 ~: O
protein localization and Sonic hedgehog signal transduction, and inhibited ciliogenesis. Thus,5 M( n2 B& B9 O& @* G
SEPT2 is part of a diffusion barrier at the base of the ciliary membrane and is essential for/ C3 ?2 W, F3 j5 k2 [+ x
retaining receptor-signaling pathways in the primary cilium.' _6 Y4 q8 h+ s1 D3 b
2. [2010 Research]Cancer Statistics
, Q3 N; \# @) V. }- @3. [2010 Research]Dendritic Cells in Systemic Lupus Erythematosus
9 |/ d# i/ M# u/ n% j- H* P1 \Heather M. Seitz0 y, @8 S0 V* G: M
Johnson County Community College, Science Division, Overland Park,
7 D% A6 V6 i% k# K; _1 CKansas, USA
6 t' ], G& k# W( PGlenn K. Matsushima
! _5 p; @- b4 G5 d: }+ NUNC Neuroscience Center, Department of Microbiology & Immunology,
; ^; ?" S/ R" s' G: {. H. o/ JProgram for Molecular Biology & Biotechnology, University of North
( m/ h) L( ]! N% v, }' F& NCarolina at Chapel Hill, Chapel Hill, North Carolina, USA) g9 Z" u$ B( m4 f
/ B0 l% G2 S2 f5 Z' kSystemic lupus erythematosus (SLE) persists as a chronic inflammatory autoimmune8 c0 F6 N- |/ i
disease and is characterized by the production of autoantibodies
1 ]' K; e1 I$ p, T- f. gand immune complexes that affect multiple organs. The underlying mechanism
& r4 a" l: @/ K8 V" |7 f8 nthat triggers and sustains disease are complex and involve certain
3 ~! w3 O9 n* g# S- E# q3 Vsusceptibility genes and environmental factors. There have been several immune j+ j) \8 ^5 F# x
mediators linked to SLE including cytokines and chemokines that have
# }, q$ ?$ W/ t% ^been reviewed elsewhere [1–3]. A number of articles have reviewed the role
$ f3 r9 ?. M- w p( E9 yof B cells and T cells in SLE [4–10]. Here, we focus on the role of dendritic$ v- h& S" v4 `( B( s. w
cells (DC) and innate immune factors that may regulate autoreactive B cells.
0 _/ H" p- j5 `4 _4. [2010 Research]Differential immunophenotypic analysis of dendritic cell tumours& I* W& |5 A# L7 g4 }
Tomohiko Orii,1,2 Hiroaki Takeda,2 Sumio Kawata,2 Kunihiko Maeda,1
6 ^5 n' I8 I. _, }Mitsunori Yamakawa1: i" M8 A e0 {4 J6 B; m
$ \1 j8 u2 `# f. ], x) X7 ^' z
ABSTRACT5 R# w- s+ B! \7 [& P: u
Aims The phenotypic and biological characteristics of, F$ O/ B7 {2 c1 \" E
dendritic cell (DC) tumours have not been fully) [' j) X( S0 H) C/ R
elucidated. The aim of this study was to compare the
9 `' P8 E! f" S5 a0 Himmunophenotypic characteristics of DC-related markers
6 S. P& D# A2 I/ p4 j- U vand cell-cycle-associated markers among DC tumours
$ R; w3 h6 a4 W; Aand finally to utilise them for differential diagnosis of DC+ r2 X$ }% @$ v; F/ d
tumours.
; g# ?- z$ Y# _( H: S" zMethods Tissue sections from 28 patients with DC& w0 \% G1 c H
tumours were immunohistochemically examined using
5 P! B5 l# s# ?; U: X( S& eDC-related and cell-cycle-associated markers.& [+ b6 ^) p% O
Results The Langerhans cell histiocytosis (LCH) and
% P1 h. A6 V; j+ DLangerhans cell sarcoma (LCS) samples were positive for8 i9 q! B) B6 F7 y, H$ D$ j
S-100 protein, CD1a, Langerin, fascin, DEC-205 and DCSIGN., E0 e( p5 N. \5 u3 o( O$ u
Interdigitating dendritic cell sarcoma (IDCS) was
0 w ~0 L! Y7 R& q0 M2 C: `- Gpositive for S-100 protein and fascin and negative for+ B0 ^, c2 z+ P i; Q1 B0 N* U
Langerin. In addition, two IDCS samples were positive for
5 j2 f5 a. y& j" U! y9 c; |* YCD1a, DEC-205 and DC-SIGN. The labelling indices of
7 P5 ?: L5 ?% z# ^7 GKi-67, cyclin A, cyclin B1 and acetylated histone H3 on the
1 N0 l$ e& w3 h0 X& uLCS and IDCS specimens were significantly higher than
1 M% f# ?8 i3 r; ~0 \those on the LCH specimens. The expression of p53 was
$ v5 R' |' ]& G0 N @also significantly higher in the LCS specimens than in the' s- @+ E0 y/ a* z9 @* j
LCH specimens. The numbers of infiltrating CD123+ and
3 L [* K2 K. e4 p9 WFOXP3+ cells were also significantly higher in the LCS
( F+ p4 H, T* k, X2 `7 s4 G7 ysamples than in the LCH and IDCS samples. Follicular
5 |. B! I5 }! [5 \" ~/ Ydendritic cell sarcoma was distinguished from other DC) _6 w2 S+ g& c6 r' G* k. `
tumours by the lack of DC-SIGN, Langerin and DCE-205.: W( j; D+ T* Y' } z
Conclusions These results suggest that Langerin can be/ G( B, R( Q/ S/ f9 S
used to distinguish LCS from IDCS, and DC-SIGN and$ ^5 @# r2 c4 }. T4 q: s
DEC-205 can be used to identify DC tumour cells. The
4 Y) t6 h1 {) C7 W% y7 Lfrequency of cell-cycle-associated markers can be used
* Q/ G# P% ~; R+ ?0 g3 |for the differential diagnosis of malignant and benign DC tumours.
8 {* W4 u; v* O1 w$ |9 B5. [2010 Research]Gut inflammation provides a respiratory electron acceptor for Salmonella
* w: S7 Y( }, C3 a0 q8 z. G, G& hSebastian E. Winter1, Parameth Thiennimitr1,2, Maria G. Winter1, Brian P. Butler1, Douglas L. Huseby3, Robert W. Crawford1,% |; b5 U9 q0 w* @
Joseph M. Russell1, Charles L. Bevins1, L. Garry Adams4, Rene′e M. Tsolis1, John R. Roth3 & Andreas J. Ba¨umler14 V8 u1 B/ V( z' c/ f# b% e+ a0 J
C5 z% o/ u4 YSalmonella enterica serotype Typhimurium (S. Typhimurium) causes acute gut inflammation by using its virulence
- e8 h7 t! _: y5 L7 G- A# P6 Nfactors to invade the intestinal epithelium and survive in mucosal macrophages. The inflammatory response
% X$ h, n$ |8 M6 benhances the transmission success of S. Typhimurium by promoting its outgrowth in the gut lumen through' l0 E* k6 R% `: @$ F6 A
unknown mechanisms. Here we show that reactive oxygen species generated during inflammation react with
8 H, P8 T4 g# N$ T- Aendogenous, luminal sulphur compounds (thiosulphate) to form a new respiratory electron acceptor, tetrathionate.8 t; r- c+ Q0 s7 Q/ ^. @+ f* G
The genes conferring the ability to use tetrathionate as an electron acceptor produce a growth advantage for S. s: B) S% a& P7 h
Typhimurium over the competing microbiota in the lumen of the inflamed gut. We conclude that S. Typhimurium
! R0 s9 V( N K4 [7 G* w0 b( c% x* @virulence factors induce host-driven production of a new electron acceptor that allows the pathogen to use0 i; k) E, S$ S% F
respiration to compete with fermenting gut microbes. Thus the ability to trigger intestinal inflammation is crucial for3 M3 F4 L9 ]. ^" u( ? x
the biology of this diarrhoeal pathogen.
4 G- E5 G& r- d6. [2010 Research]Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels" @! b& ^4 @" G8 O; ?% D% m2 D* Z+ J
Bertrand Coste,1 Jayanti Mathur,2 Manuela Schmidt,1 Taryn J. Earley,1 Sanjeev Ranade,13 e. w% z- f: f L7 L
Matt J. Petrus,2 Adrienne E. Dubin,1 Ardem Patapoutian1,2*
# m0 Z& x; A9 h$ r5 y& W7 p! ~% Q6 w8 U# u6 ~, `" Q; x
Mechanical stimuli drive many physiological processes, including touch and pain sensation,- D6 p% F( G/ G- x
hearing, and blood pressure regulation. Mechanically activated (MA) cation channel activities5 ]( z$ a# ?3 Y$ R
have been recorded in many cells, but the responsible molecules have not been identified.
. S( O$ ^( u; i1 R X* wWe characterized a rapidly adapting MA current in a mouse neuroblastoma cell line. Expression) a S9 S" S- C2 ^5 i+ \+ W! G
profiling and RNA interference knockdown of candidate genes identified Piezo1 (Fam38A) to be, [' e( T1 R @' d6 V) h; v
required for MA currents in these cells. Piezo1 and related Piezo2 (Fam38B) are vertebrate
3 q" l$ [, ^5 R* Y ymultipass transmembrane proteins with homologs in invertebrates, plants, and protozoa.( M1 o, t! G/ A
Overexpression of mouse Piezo1 or Piezo2 induced two kinetically distinct MA currents. Piezos( E7 \! Z* s" g* s( D# X F' K
are expressed in several tissues, and knockdown of Piezo2 in dorsal root ganglia neurons
8 p( }0 @ _1 Especifically reduced rapidly adapting MA currents. We propose that Piezos are components of/ B7 H2 E! Z) D) G
MA cation channels.
4 v6 x+ c R' K- t7 P5 D7. [2010 Research]Platelets Amplify Inflammation in Arthritis via Collagen-Dependent Microparticle Production7 g# C) s" b( N7 f
Eric Boilard,1 Peter A. Nigrovic,1,2 Katherine Larabee,1 Gerald F. M. Watts,1
& M0 L& {1 `2 n8 YJonathan S. Coblyn,1 Michael E. Weinblatt,1 Elena M. Massarotti,16 f# A( `1 n6 L0 h' W
Eileen Remold-O’Donnell,3 Richard W. Farndale,4 Jerry Ware,5 David M. Lee1*% u, q3 ?. B. G& ?" ?3 s
3 q, J6 J! f/ d- R% L \0 ^; d# ^/ {In addition to their pivotal role in thrombosis and wound repair, platelets participate in' F, Y6 _4 F5 [# _+ M7 \" N4 B) f8 @, c
inflammatory responses. We investigated the role of platelets in the autoimmune disease
/ S' q o! p) D1 ~ p+ T4 _7 w& erheumatoid arthritis. We identified platelet microparticles—submicrometer vesicles elaborated by% P0 C+ N+ C7 j
activated platelets—in joint fluid from patients with rheumatoid arthritis and other forms of
& e) o; _( W; r% R# _inflammatory arthritis, but not in joint fluid from patients with osteoarthritis. Platelet: g" Z1 b' w( j3 s$ Z3 ~& U& @
microparticles were proinflammatory, eliciting cytokine responses from synovial fibroblasts via
5 K- y: I! I& t. v3 r3 D# r3 ginterleukin-1. Consistent with these findings, depletion of platelets attenuated murine
3 X8 A0 m( c9 ^inflammatory arthritis. Using both pharmacologic and genetic approaches, we identified the" S- F; b# q- X; `3 R9 [
collagen receptor glycoprotein VI as a key trigger for platelet microparticle generation in arthritis
/ P2 R5 g( k9 n t1 Y% }# Apathophysiology. Thus, these findings demonstrate a previously unappreciated role for platelets. }" ?9 B1 n6 \/ b$ }; v
and their activation-induced microparticles in inflammatory joint diseases.0 X" v5 F( \) g5 b" T
8. [2010 Research]The architecture of respiratory complex I
! ]; @6 D6 C; [Rouslan G. Efremov*, Rozbeh Baradaran* & Leonid A. Sazanov" F' d- s; x6 `
& Z* }/ k7 ~6 i5 _; [* s7 ^
Complex I is the first enzyme of the respiratory chain and has a central role in cellular energy production, coupling electron
1 E( C( j% a+ \) F0 C( ktransfer between NADH and quinone to proton translocation by an unknown mechanism. Dysfunction of complex I has been+ C8 m) a$ U, Q
implicated in many human neurodegenerative diseases. We have determined the structure of its hydrophilic domain, u7 ^0 O8 r* ~6 Y) [, z9 L- W
previously. Here, we report the a-helical structure of the membrane domain of complex I from Escherichia coli at 3.9A°! i% }& a0 F- e4 i# z/ r$ M
resolution. The antiporter-like subunits NuoL/M/Neach contain 14 conserved transmembrane (TM) helices. Two of them are& D9 @& Q1 g7 r/ t
discontinuous, as in some transporters. Unexpectedly, subunit NuoL also contains a 110-A° long amphipathic a-helix, spanning
) K$ w) H/ g. N. e/ dalmost the entire length of the domain. Furthermore, we have determined the structure of the entire complex I from Thermus
) s- f8 C& D1 N6 Jthermophilus at 4.5A°1 o; r* e6 p0 b- f1 B2 l
resolution. The L-shaped assembly consists of the a-helicalmodel for themembrane domain, with 63TM
& D& q" A* ]5 z0 C6 z0 c! s8 \helices, and the known structure of the hydrophilic domain. The architecture of the complex provides strong clues about the# T* t& m4 E4 x
coupling mechanism: the conformational changes at the interface of the two main domains may drive the long amphipathic4 ], C) D$ c# E5 f
a-helix of NuoL in a piston-like motion, tilting nearby discontinuous TM helices, resulting in proton translocation.
' `* l/ u4 P9 U" |! k5 U[hide][/hide] |
附件: 你需要登录才可以下载或查看附件。没有帐号？注册
-
总评分: 威望 + 5
包包 + 20
查看全部评分
|
发表于 2011-5-5 23:53
谢谢