http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : ( Myriam Gorospe ) (검색결과 5 건)
- 무료
- 기관 내 무료
- 유료
-
-
Mitochondrial noncoding RNA transport
( Kyoung Mi Kim ),( Ji Heon Noh ),( Kotb Abdelmohsen ),( Myriam Gorospe ) 생화학분자생물학회(구 한국생화학분자생물학회) 2017 BMB Reports Vol.50 No.4
Mitochondria are cytosolic organelles essential for generating energy and maintaining cell homeostasis. Despite their critical function, the handful of proteins expressed by the mitochondrial genome is insufficient to maintain mitochondrial structure or activity. Accordingly, mitochondrial metabolism is fully dependent on factors encoded by the nuclear DNA, including many proteins synthesized in the cytosol and imported into mitochondria via established mechanisms. However, there is growing evidence that mammalian mitochondria can also import cytosolic noncoding RNA via poorly understood processes. Here, we summarize our knowledge of mitochondrial RNA, discuss recent progress in understanding the molecular mechanisms and functional impact of RNA import into mitochondria, and identify rising challenges and opportunities in this rapidly evolving field. [BMB Reports 2017; 50(4): 164-174]
-
MicroRNA-146a Suppresses Metastatic Activity in Brain Metastasis
황수진,김현호,Ho Jun Seol,박영미,Kang Ho Kim,Myriam Gorospe,남도현 한국분자세포생물학회 2012 Molecules and cells Vol.34 No.3
Primary lung tumors, breast tumors, and melanoma me-tastasize mainly in the brain where therapy is limited to surgery and radiation. To investigate the molecular basis of brain metastases, we isolated brain-trophic metastatic MDA-MB-435-LvBr2 (LvBr2) cells via left ventricle (LV) injection of MDA-MB-435 cells into immunodeficiency (NOD/ SCID) mice. Whereas parent MDA-MB-435 cells displayed an elongated morphology, LvBr2 cells were round and displayed an aggregated distribution. LvBr2 cells expressed lower beta-catenin levels and higher heterogeneous nuclear ribonucleoprotein C1/C2 (hnRNPC) levels than parental cells. Since microRNAs are known to play an important role in cancer progression including metastasis, we screened microRNAs expressed specifically in brain metastases. MicroRNA-146a was almost undetectable in LvBr2 cells and highly expressed in the parental cells. Overexpression of miR-146a increased beta-catenin expression and suppressed the migratory and invasive activity of LvBr2 cells. The miR-146a-elicited decrease in hnRNPC in turn lowered the expression of MMP-1, uPA, and uPAR and inhibited the migratory and invasive activity of LvBr2 cells. Taken together, our findings indicate that miR-146a is virtually absent from brain metastases and can suppress their metastatic potential including their migratory and invasive activities associated with upregulation of beta-catenin and downregulation of hnRNPC.
-
Kim, Chongtae,Kim, Wook,Lee, Heejin,Ji, Eunbyul,Choe, Yun-Jeong,Martindale, Jennifer L.,Akamatsu, Wado,Okano, Hideyuki,Kim, Ho-Shik,Nam, Suk Woo,Gorospe, Myriam,Lee, Eun Kyung American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.1
<P>Tight regulation of autophagy is critical for the fate of pancreatic β cells. The autophagy protein ATG5 is essential for the formation of autophagosomes by promoting the lipidation of microtubule-associated protein LC3 (light chain 3). However, little is known about the mechanisms that regulate ATG5 expression levels. In this study, we investigated the regulation of ATG5 expression by HuD. The association of HuD with <I>ATG5</I> mRNA was analyzed by ribonucleoprotein complex immunoprecipitation and biotin pulldown assays. HuD expression levels in pancreatic β cells were knocked down via siRNA, elevated by overexpression of a HuD-expressing plasmid. The expression levels of HuD, ATG5, LC3, and β-actin were determined by Western blot and quantitative RT-PCR analysis. Autophagosome formation was assessed by fluorescence microscopy in GFP-LC3-expressing cells and in pancreatic tissues from WT and HuD-null mice. We identified <I>ATG5</I> mRNA as a post-transcriptional target of the mammalian RNA-binding protein HuD in pancreatic β cells. HuD associated with the 3′-UTR of the <I>ATG5</I> mRNA. Modulating HuD abundance did not alter <I>ATG5</I> mRNA levels, but HuD silencing decreased <I>ATG5</I> mRNA translation, and, conversely, HuD overexpression enhanced <I>ATG5</I> mRNA translation. Through its effect on ATG5, HuD contributed to the lipidation of LC3 and the formation of LC3-positive autophagosomes. In keeping with this regulatory paradigm, HuD-null mice displayed lower ATG5 and LC3 levels in pancreatic β cells. Our results reveal HuD to be an inducer of ATG5 expression and hence a critical regulator of autophagosome formation in pancreatic β cells.</P>
-
miR-431 promotes differentiation and regeneration of old skeletal muscle by targeting <i>Smad4</i>
Lee, Kwang-Pyo,Shin, Yeo Jin,Panda, Amaresh C.,Abdelmohsen, Kotb,Kim, Ji Young,Lee, Seung-Min,Bahn, Young Jae,Choi, Jeong Yi,Kwon, Eun-Soo,Baek, Su-Jin,Kim, Seon-Young,Gorospe, Myriam,Kwon, Ki-Sun Cold Spring Harbor Laboratory Press 2015 Genes & development Vol.29 No.15
<P>Lee et al. show that elevating miR-431 improved the myogenic capacity of old myoblasts, while inhibiting endogenous miR-431 lowered myogenesis. In an in vivo model of muscle regeneration following cardiotoxin injury, ectopic miR-431 injection greatly improved muscle regeneration and reduced SMAD4 levels.</P><P>The myogenic capacity of myoblasts decreases in skeletal muscle with age. In addition to environmental factors, intrinsic factors are important for maintaining the regenerative potential of muscle progenitor cells, but their identities are largely unknown. Here, comparative analysis of microRNA (miRNA) expression profiles in young and old myoblasts uncovered miR-431 as a novel miRNA showing markedly reduced abundance in aged myoblasts. Importantly, elevating miR-431 improved the myogenic capacity of old myoblasts, while inhibiting endogenous miR-431 lowered myogenesis. Bioinformatic and biochemical analyses revealed that miR-431 directly interacted with the 3′ untranslated region (UTR) of <I>Smad4</I> mRNA, which encodes one of the downstream effectors of TGF-β signaling. In keeping with the low levels of miR-431 in old myoblasts, SMAD4 levels increased in this myoblast population. Interestingly, in an in vivo model of muscle regeneration following cardiotoxin injury, ectopic miR-431 injection greatly improved muscle regeneration and reduced SMAD4 levels. Consistent with the finding that the mouse miR-431 seed sequence in the <I>Smad4</I> 3′ UTR is conserved in the human <I>SMAD4</I> 3′ UTR, inhibition of miR-431 also repressed the myogenic capacity of human skeletal myoblasts. Taken together, our results suggest that the age-associated miR-431 plays a key role in maintaining the myogenic ability of skeletal muscle with age.</P>
KISS연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
