A stress-induced response complex (SIRC) shuttles miRNAs, siRNAs, and oligonucleotides to the nucleus

Although some information is available for specific subsets of miRNAs and several factors have been shown to bind oligonucleotides (ONs), no general transport mechanism for these molecules has been identified to date. In this work, we demonstrate that the nuclear transport of ONs, siRNAs, and miRNAs responds to cellular stress. Furthermore, we have identified a stress-induced response complex (SIRC), which includes Ago-1 and Ago-2 in addition to the transcription and splicing regulators YB1, CTCF, FUS, Smad1, Smad3, and Smad4. The SIRC transports endogenous miRNAs, siRNAs, and ONs to the nucleus. We show that cellular stress can significantly increase ON- or siRNA-directed splicing switch events and endogenous miRNA targeting of nuclear RNAs.

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mDia2 Shuttles between the Nucleus and the Cytoplasm through the Importin-α/β- and CRM1-mediated Nuclear Transport Mechanism

Journal of Biological Chemistry ◽

10.1074/jbc.m806191200 ◽

2008 ◽

Vol 284 (9) ◽

pp. 5753-5762 ◽

Cited By ~ 37

Author(s):

Takashi Miki ◽

Katsuya Okawa ◽

Toshihiro Sekimoto ◽

Yoshihiro Yoneda ◽

Sadanori Watanabe ◽

...

Keyword(s):

Transport Mechanism ◽

Nuclear Transport ◽

Importin Α

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TEM Study and Hall Measurement of nc-Si Prepared by Controlled Deposition

MRS Proceedings ◽

10.1557/proc-283-591 ◽

1992 ◽

Vol 283 ◽

Cited By ~ 8

Author(s):

Masami Nakata ◽

Isamu Shimizu

Keyword(s):

Electrical Transport ◽

Transport Mechanism ◽

Crystalline Silicon ◽

Nanocrystalline Silicon ◽

Dominant Factor ◽

Microscopic Structure ◽

Hall Effect Measurements ◽

Sample Structure ◽

Controlled Deposition ◽

General Transport

ABSTRACTWe report the results of a study in which we combined growth experiments with measurements of the nc-structure and of electrical transport Samples were prepared by plasma enhanced-CVD using SiF4 and H2 gases. We also added PH3 and H2 as control parameters for structural change. The microscopic structure was directly observed by TEM. Electron transport in nc-Si was investigated by Hall effect measurements performed at temperatures from 100K to 400K. We produced samples in which the Hall mobility was applied from general transport mechanism of poly crystalline silicon. However, from TEM observation, we conclude that dominant factor on electrical transport strongly depends on the sample structure, and nanocrystalline-silicon structure is so varied as to make it difficult to determine the transport mechanism without the observation of the microscopic structure.

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The level of intracellular glutathione is a key regulator for the induction of stress-activated signal transduction pathways including Jun N-terminal protein kinases and p38 kinase by alkylating agents.

Molecular and Cellular Biology ◽

10.1128/mcb.17.8.4792 ◽

1997 ◽

Vol 17 (8) ◽

pp. 4792-4800 ◽

Cited By ~ 164

Author(s):

D Wilhelm ◽

K Bender ◽

A Knebel ◽

P Angel

Keyword(s):

Protein Kinases ◽

Nuclear Dna ◽

Alkylating Agents ◽

Cellular Stress ◽

Critical Role ◽

Cellular Stress Response ◽

Mitogen Activated Protein Kinase ◽

Irradiation Damage ◽

Induced Response ◽

Intracellular Glutathione

Monofunctional alkylating agents like methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) are potent inducers of cellular stress leading to chromosomal aberrations, point mutations, and cell killing. We show that these agents induce a specific cellular stress response program which includes the activation of Jun N-terminal kinases/stress-activated protein kinases (JNK/SAPKs), p38 mitogen-activated protein kinase, and the upstream kinase SEK1/MKK4 and which depends on the reaction mechanism of the alkylating agent in question. Similar to another inducer of cellular stress, UV irradiation, damage of nuclear DNA by alkylation is not involved in the MMS-induced response. However, in contrast to UV and other inducers of the JNK/SAPKs and p38 pathways, activation of growth factor and G-protein-coupled receptors does not play a role in the MMS response. We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS. In light of the JNK/SAPK-dependent induction of c-jun and c-fos transcription, and the Jun/Fos-induced transcription of xenobiotic-metabolizing enzymes, these data provide a potential critical role of JNK/SAPK and p38 in the induction of a cellular defense program against cytotoxic xenobiotics such as MMS.

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Cellular stress stimulates nuclear localization signal (NLS) independent nuclear transport of MRJ

Experimental Cell Research ◽

10.1016/j.yexcr.2012.03.024 ◽

2012 ◽

Vol 318 (10) ◽

pp. 1086-1093 ◽

Cited By ~ 8

Author(s):

Joel F. Andrews ◽

Landon J. Sykora ◽

Tiasha Barik Letostak ◽

Mitchell E. Menezes ◽

Aparna Mitra ◽

...

Keyword(s):

Nuclear Localization ◽

Nuclear Localization Signal ◽

Nuclear Transport ◽

Cellular Stress ◽

Localization Signal

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Effects of Vincristine on Endothelial Microtubules in the Spinal Cord

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100090270 ◽

1976 ◽

Vol 34 ◽

pp. 58-59

Author(s):

John L. Beggs ◽

John D. Waggener ◽

Wanda Miller

Keyword(s):

Spinal Cord ◽

Biological Activity ◽

Horseradish Peroxidase ◽

Transport Mechanism ◽

Vasogenic Edema ◽

Vesicular Transport ◽

Close Proximity

Microtubules (MT) are versatile organelles participating in a wide variety of biological activity. MT involvement in the movement and transport of cytoplasmic components has been well documented. In the course of our study on trauma-induced vasogenic edema in the spinal cord we have concluded that endothelial vesicles contribute to the edema process. Using horseradish peroxidase as a vascular tracer, labeled endothelial vesicles were present in all situations expected if a vesicular transport mechanism was in operation. Frequently,labeled vesicles coalesced to form channels that appeared to traverse the endothelium. The presence of MT in close proximity to labeled vesicles sugg ested that MT may play a role in vesicular activity.

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A microscopic marker experiment study on high temperature oxidation of Ni-Al alloy

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100144085 ◽

1986 ◽

Vol 44 ◽

pp. 514-515

Author(s):

Shou-kong Fan

Keyword(s):

Transport Mechanism ◽

High Temperature Oxidation ◽

Transverse Section ◽

Al Alloy ◽

Metal Interface ◽

Electron Microscopic ◽

Temperature Oxidation ◽

Analytical Electron ◽

Microscopic Studies ◽

First Time

Transmission and analytical electron microscopic studies of scale microstructures and microscopic marker experiments have been carried out in order to determine the transport mechanism in the oxidation of Ni-Al alloy. According to the classical theory, the oxidation of nickel takes place by transport of Ni cations across the scale forming new oxide at the scale/gas interface. Any markers deposited on the Ni surface are expected to remain at the scale/metal interface after oxidation. This investigation using TEM transverse section techniques and deposited microscopic markers shows a different result,which indicates that a considerable amount of oxygen was transported inward. This is the first time that such fine-scale markers have been coupled with high resolution characterization instruments such as TEM/STEM to provide detailed information about evolution of oxide scale microstructure.

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Nuclear transport: never-ending cycles of signals and receptors

Essays in Biochemistry ◽

10.1042/bse0360089 ◽

2000 ◽

Vol 36 ◽

pp. 89-103 ◽

Cited By ~ 8

Author(s):

Dianne M. Barry ◽

Susan R. Wente

Keyword(s):

Nuclear Transport

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Mitochondrial hyperfusion: a friend or a foe

Biochemical Society Transactions ◽

10.1042/bst20190987 ◽

2020 ◽

Vol 48 (2) ◽

pp. 631-644 ◽

Cited By ~ 3

Author(s):

Rajdeep Das ◽

Oishee Chakrabarti

Keyword(s):

Negative Impact ◽

Cellular Stress ◽

Cellular Homeostasis ◽

Mitochondrial Population

The cellular mitochondrial population undergoes repeated cycles of fission and fusion to maintain its integrity, as well as overall cellular homeostasis. While equilibrium usually exists between the fission–fusion dynamics, their rates are influenced by organellar and cellular metabolic and pathogenic conditions. Under conditions of cellular stress, there is a disruption of this fission and fusion balance and mitochondria undergo either increased fusion, forming a hyperfused meshwork or excessive fission to counteract stress and remove damaged mitochondria via mitophagy. While some previous reports suggest that hyperfusion is initiated to ameliorate cellular stress, recent studies show its negative impact on cellular health in disease conditions. The exact mechanism of mitochondrial hyperfusion and its role in maintaining cellular health and homeostasis, however, remain unclear. In this review, we aim to highlight the different aspects of mitochondrial hyperfusion in either promoting or mitigating stress and also its role in immunity and diseases.

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