Untitled

Shrode, Lamara D.; Tapper, Hans; Grinstein, Sergio

doi:10.1023/a:1022407116339

Cited by 174 publications

(43 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Apoptotic stimulimediated nuclear trafficking represents a proapoptotic pathway used to maximize the efficiency of committed cell death in multiple cell compartments. We now show that CLIC4 translocates to the nucleus, and its presence may participate in alteration of pH and chloride ion content that could be involved in the apoptotic events in the nucleus, such as activation of nucleases and DNA fragmentation (33)(34)(35). Our EM studies find CLIC4 localized to the nuclear membrane, and in preliminary studies we have evidence that CLIC4 translocation is FIG.…”

Section: Mtclic/clic4 Nuclear Translocation Initiates Apoptosismentioning

confidence: 52%

The Organellular Chloride Channel Protein CLIC4/mtCLIC Translocates to the Nucleus in Response to Cellular Stress and Accelerates Apoptosis

Suh¹,

Mutoh²,

Nagashima

et al. 2004

Journal of Biological Chemistry

132

150

View full text Add to dashboard Cite

CLIC4/mtCLIC, a chloride intracellular channel protein, localizes to the mitochondria and cytoplasm of keratinocytes and participates in the apoptotic response to stress. We now show that multiple stress inducers cause the translocation of cytoplasmic CLIC4 to the nucleus. Immunogold electron microscopy and confocal analyses indicate that nuclear CLIC4 is detected prior to the apoptotic phenotype. CLIC4 associates with the Ran, NTF2, and Importin-␣ nuclear import complexes in immunoprecipitates of lysates from cells treated with apoptotic/stress-inducing agents. Deletion or mutation of the nuclear localization signal in the C terminus of CLIC4 eliminates nuclear translocation, whereas N terminus deletion enhances nuclear localization. Targeting CLIC4 to the nucleus via adenoviral transduction accelerates apoptosis when compared with cytoplasmic CLIC4, and only nuclear-targeted CLIC4 causes apoptosis in Apaf null mouse fibroblasts or in Bcl-2-overexpressing keratinocytes. These results indicate that CLIC4 nuclear translocation is an integral part of the cellular response to stress and may contribute to the initiation of nuclear alterations that are associated with apoptosis.

show abstract

Section: Mtclic/clic4 Nuclear Translocation Initiates Apoptosismentioning

confidence: 52%

The Organellular Chloride Channel Protein CLIC4/mtCLIC Translocates to the Nucleus in Response to Cellular Stress and Accelerates Apoptosis

Suh¹,

Mutoh²,

Nagashima

et al. 2004

Journal of Biological Chemistry

132

150

View full text Add to dashboard Cite

show abstract

“…pH is also one of the factors thought to control the rate of cell proliferation and transformation (45). In many tumor cell lines pH i is more alkaline than in normal cells (46).…”

Section: Discussionmentioning

confidence: 99%

Association of Plasminogen with Dipeptidyl Peptidase IV and Na+/H+ Exchanger Isoform NHE3 Regulates Invasion of Human 1-LN Prostate Tumor Cells

Gonzalez-Gronow

Misra

Gawdi

et al. 2005

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…control of cellular function [80,81]. There is especially a hibiting more or less distinct pH optima.…”

Section: Methodsmentioning

confidence: 99%

ZnO nanowires: chemical growth, electrodeposition, and application to intracellular nano‐sensors

Willander

Klason

Yang

et al. 2008

Phys. Status Solidi (c)

View full text Add to dashboard Cite

In this paper we present our results on growth, characterization, and nano‐devices based on ZnO nano‐structures. The ZnO nano‐structures were grown by mainly two methods, the catalytic Vapor Liquid Solid (VLS) and the low temperature chemical growth. We show that by multiple coating combined with low temperature chemical growth, well aligned with size controlled ZnO nanowires on silicon substrates can be achieved. The dissolution, due to its important on the stability of ZnO nano‐structures in aqueous medium, is then discussed and some preliminary experimental results are shown. Basic Optical characteristics of ZnO nano‐rods are briefly discussed. Finally, electrochemical intracellular nano‐sensors based on ZnO nano‐wires are demonstrated as efficient nano‐sensors for monitoring the human cell activity with minute pH changes. (© 2008 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)

show abstract

Untitled

Cited by 174 publications

References 46 publications

The Organellular Chloride Channel Protein CLIC4/mtCLIC Translocates to the Nucleus in Response to Cellular Stress and Accelerates Apoptosis

The Organellular Chloride Channel Protein CLIC4/mtCLIC Translocates to the Nucleus in Response to Cellular Stress and Accelerates Apoptosis

Association of Plasminogen with Dipeptidyl Peptidase IV and Na+/H+ Exchanger Isoform NHE3 Regulates Invasion of Human 1-LN Prostate Tumor Cells

ZnO nanowires: chemical growth, electrodeposition, and application to intracellular nano‐sensors

Contact Info

Product

Resources

About