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Showing 1-12 of 12 results for "CSTZFN" within Papers

Persistent activation of Nrf2 through p62 in hepatocellular carcinoma cells.

Yoshihiro Inami et al.

The Journal of cell biology, 193(2), 275-284 (2011-04-13)

Suppression of autophagy is always accompanied by marked accumulation of p62, a selective autophagy substrate. Because p62 interacts with the Nrf2-binding site on Keap1, which is a Cullin 3-based ubiquitin ligase adapter protein, autophagy deficiency causes competitive inhibition of the

Loss of Bace2 in zebrafish affects melanocyte migration and is distinct from Bace1 knock out phenotypes.

Frauke van Bebber et al.

Journal of neurochemistry, 127(4), 471-481 (2013-02-15)

Alzheimer's disease is the most frequent dementia. Pathologically, Alzheimer's disease is characterized by the accumulation of senile plaques composed of amyloid β-peptide (Aβ). Two proteases, β- and γ-secretase proteolytically generate Aβ from its precursor, the ß-amyloid precursor protein (APP). Inhibition

Systematic identification of functional residues in mammalian histone H2AX.

Wei-Ta Chen et al.

Molecular and cellular biology, 33(1), 111-126 (2012-10-31)

The histone variant H2AX is a principal component of chromatin involved in the detection, signaling, and repair of DNA double-strand breaks (DSBs). H2AX is thought to operate primarily through its C-terminal S139 phosphorylation, which mediates the recruitment of DNA damage

orco mutant mosquitoes lose strong preference for humans and are not repelled by volatile DEET.

Matthew DeGennaro et al.

Nature, 498(7455), 487-491 (2013-05-31)

Female mosquitoes of some species are generalists and will blood-feed on a variety of vertebrate hosts, whereas others display marked host preference. Anopheles gambiae and Aedes aegypti have evolved a strong preference for humans, making them dangerously efficient vectors of

Resilient immortals, characterizing and utilizing Bax/Bak deficient Chinese hamster ovary (CHO) cells for high titer antibody production.

Shahram Misaghi et al.

Biotechnology progress, 29(3), 727-737 (2013-04-19)

Cell death due to apoptosis is frequently observed in large-scale manufacturing of therapeutic proteins, and can reduce product accumulation in bioreactors. Several different strategies that involve overexpression of antiapoptotic or downregulation of proapoptotic proteins have been designed in attempt to

A novel therapeutic molecule against HTLV-1 infection targeting provirus.

A Tanaka et al.

Leukemia, 27(8), 1621-1627 (2013-02-16)

Human T-cell leukemia virus type 1 (HTLV-1), which causes adult T-cell leukemia (ATL) in humans, establishes a life-long latent infection. Current therapies are not very effective against HTLV-1-associated disorders. A novel therapeutic approach may help to combat HTLV-1 infection. A

Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth.

Bettina Schmid et al.

Proceedings of the National Academy of Sciences of the United States of America, 110(13), 4986-4991 (2013-03-05)

Mutations in the Tar DNA binding protein of 43 kDa (TDP-43; TARDBP) are associated with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with TDP-43(+) inclusions (FTLD-TDP). To determine the physiological function of TDP-43, we knocked out zebrafish Tardbp and

A requirement for wild-type Ras isoforms in mutant KRas-driven signalling and transformation.

Carolyn Bentley et al.

The Biochemical journal, 452(2), 313-320 (2013-03-19)

The mutant forms of KRas, NRas and HRas drive the initiation and progression of a number of human cancers, but less is known about the role of WT (wild-type) Ras alleles and isoforms in cancer. We used zinc-finger nucleases targeting

PARP1 is required for chromosomal translocations.

Justin Wray et al.

Blood, 121(21), 4359-4365 (2013-04-10)

Chromosomal translocations are common contributors to malignancy, yet little is known about the precise molecular mechanisms by which they are generated. Sequencing translocation junctions in acute leukemias revealed that the translocations were likely mediated by a DNA double-strand break repair

Genetic mutation of recombination activating gene 1 in Dahl salt-sensitive rats attenuates hypertension and renal damage.

David L Mattson et al.

American journal of physiology. Regulatory, integrative and comparative physiology, 304(6), R407-R414 (2013-02-01)

Hypertension and renal damage in Dahl SS rats are associated with increased infiltrating immune cells in the kidney. To examine the role of infiltrating immune cells in this disease process, a zinc finger nuclease targeting bases 672-706 of recombination-activating gene

Zinc Finger Nuclease induced DNA double stranded breaks and rearrangements in MLL.

To Uyen Do et al.

Mutation research, 740(1-2), 34-42 (2013-01-08)

Radiation treatment or chemotherapy has been linked with a higher risk of secondary cancers such as therapy related Acute Myeloid Leukemia (tAML). Several of these cancers have been shown to be correlated to the introduction of double stranded breaks (DSB)

Heterozygous knockout of transforming growth factor-β1 protects Dahl S rats against high salt-induced renal injury.

Chun Cheng Andy Chen et al.

Physiological genomics, 45(3), 110-118 (2012-12-20)

The present study employed a zinc-finger nuclease strategy to create heterozygous knockout (KO) rats for the transforming growth factor-β1 (Tgfb1) gene on the Dahl SS/Jr genetic background (TGF-β1(+/-) Dahl S). Intercrossing TGF-β1(+/-) rats did not produce any homozygous KO rats

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