Filtered By:
Condition: Ataxia

This page shows you your search results in order of date. This is page number 5.

Order by Relevance | Date

Total 67 results found since Jan 2013.

Polycation-functionalized nanoporous silicon particles for gene silencing on breast cancer cells.
Abstract Nanoporous silicon particles (pSi), with a pore size in the range of 20-60 nm, were modified with polyethyleneimine (PEI) to yield pSi-PEI particles, which were subsequently complexed with siRNA. Thus, pSi-PEI/siRNA particles were fabricated, with the PEI/siRNA nanocomplexes mainly anchored inside the nanopore of the pSi particles. These hybrid particles were used as carriers to deliver siRNA to human breast cancer cells. Due to the gradual degradation of the pSi matrix under physiological conditions, the PEI/siRNA nanocomplexes were released from the pore interior in a sustained manner. Physicochemical ...
Source: Biomaterials - October 5, 2013 Category: Materials Science Authors: Zhang M, Xu R, Xia X, Yang Y, Gu J, Qin G, Liu X, Ferrari M, Shen H Tags: Biomaterials Source Type: research

Mutant γPKC that causes spinocerebellar ataxia type 14 upregulates Hsp70, which protects cells from the mutant's cytotoxicity.
Abstract Several missense mutations in the protein kinase Cγ (γPKC) gene have been found to cause spinocerebellar ataxia type 14 (SCA14), an autosomal dominant neurodegenerative disease. We previously demonstrated that the mutant γPKC found in SCA14 is misfolded, susceptible to aggregation and cytotoxic. Molecular chaperones assist the refolding and degradation of misfolded proteins and prevention of the proteins' aggregation. In the present study, we found that the expression of mutant γPKC-GFP increased the levels of heat-shock protein 70 (Hsp70) in SH-SY5Y cells. To elucidate the role of this elevation, we ...
Source: Biochemical and Biophysical Research communications - September 7, 2013 Category: Biochemistry Authors: Ogawa K, Seki T, Onji T, Adachi N, Tanaka S, Hide I, Saito N, Sakai N Tags: Biochem Biophys Res Commun Source Type: research

MELK Decreases Replication Stress Cell Biology
Maternal embryonic leucine zipper kinase (MELK) belongs to the subfamily of AMP-activated Ser/Thr protein kinases. The expression of MELK is very high in glioblastoma-type brain tumors, but it is not clear how this contributes to tumor growth. Here we show that the siRNA-mediated loss of MELK in U87 MG glioblastoma cells causes a G1/S phase cell cycle arrest accompanied by cell death or a senescence-like phenotype that can be rescued by the expression of siRNA-resistant MELK. This cell cycle arrest is mediated by an increased expression of p21WAF1/CIP1, an inhibitor of cyclin-dependent kinases, and is associated with the h...
Source: Journal of Biological Chemistry - August 16, 2013 Category: Chemistry Authors: Kig, C., Beullens, M., Beke, L., Van Eynde, A., Linders, J. T., Brehmer, D., Bollen, M. Tags: Signal Transduction Source Type: research

Nuclear Import of HBXIP Requires Collaboration with c-Fos Gene Regulation
Aberrant nuclear localization of oncogenic transcription factors and coactivators always leads to the development of cancer. We have reported that the oncoprotein hepatitis B X-interacting protein (HBXIP) acts as a novel transcriptional coactivator to promote proliferation and migration of breast cancer cells. However, the mechanism of regulating the nuclear import of HBXIP remains unclear. In the present study, we found that HBXIP interacted with c-Fos through their leucine zipper domains in vitro and in vivo. Interestingly, the leucine zipper mutant of HBXIP (or c-Fos) was unavailable to bind to c-Fos (or HBXIP), resulti...
Source: Journal of Biological Chemistry - June 28, 2013 Category: Chemistry Authors: Zhang, Y., Zhao, Y., Li, H., Li, Y., Cai, X., Shen, Y., Shi, H., Li, L., Liu, Q., Zhang, X., Ye, L. Tags: Cell Biology Source Type: research

Prelamin a accelerates vascular calcification via activation of the DNA damage response and senescence-associated secretory phenotype in vascular smooth muscle cells.
Conclusions: Prelamin A promotes VSMC calcification and aging by inducing persistent DNA damage signaling, which acts upstream of VSMC osteogenic differentiation and the senescence-associated secretory phenotype. Agents that target the DNA damage response and prelamin A toxicity may be potential therapies for the treatment of vascular calcification. PMID: 23564641 [PubMed - in process]
Source: Circulation Research - May 10, 2013 Category: Cardiology Authors: Liu Y, Drozdov I, Shroff R, Beltran LE, Shanahan CM Tags: Circ Res Source Type: research

Ca2+ and Glu Signaling in FMR1 preCGG Astrocytes Neurobiology
Premutation CGG repeat expansions (55–200 CGG repeats; preCGG) within the fragile X mental retardation 1 (FMR1) gene can cause fragile X-associated tremor/ataxia syndrome. Defects in early neuronal migration and morphology, electrophysiological activity, and mitochondria trafficking have been described in a premutation mouse model, but whether preCGG mutations also affect astrocyte function remains unknown. PreCGG cortical astrocytes (∼170 CGG repeats) displayed 3-fold higher Fmr1 mRNA and 30% lower FMR1 protein (FMRP) when compared with WT. PreCGG astrocytes showed modest reductions in expression of glutamate (Glu) tr...
Source: Journal of Biological Chemistry - May 10, 2013 Category: Chemistry Authors: Cao, Z., Hulsizer, S., Cui, Y., Pretto, D. L., Kim, K. H., Hagerman, P. J., Tassone, F., Pessah, I. N. Tags: Molecular Bases of Disease Source Type: research

Oxidative DNA damage is involved in ochratoxin A-induced G2 arrest through ataxia telangiectasia-mutated (ATM) pathways in human gastric epithelium GES-1 cells in vitro.
In conclusion, the results of this study suggested that OTA-induced oxidative DNA damage triggered the ATM-dependent pathways, which ultimately elicited a G2 arrest in GES-1 cells. PMID: 23515941 [PubMed - as supplied by publisher]
Source: Archives of Toxicology - March 21, 2013 Category: Toxicology Authors: Cui J, Liu J, Wu S, Wang Y, Shen H, Xing L, Wang J, Yan X, Zhang X Tags: Arch Toxicol Source Type: research