ABE387

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Showing 1-8 of 8 results for "ABE387" within Papers

A forward genetic screen reveals novel independent regulators of ULBP1, an activating ligand for natural killer cells.

Benjamin G Gowen et al.

eLife, 4 (2015-11-14)

Recognition and elimination of tumor cells by the immune system is crucial for limiting tumor growth. Natural killer (NK) cells become activated when the receptor NKG2D is engaged by ligands that are frequently upregulated in primary tumors and on cancer

A drug repurposing strategy for overcoming human multiple myeloma resistance to standard-of-care treatment.

Katarina Chroma et al.

Cell death & disease, 13(3), 203-203 (2022-03-06)

Despite several approved therapeutic modalities, multiple myeloma (MM) remains an incurable blood malignancy and only a small fraction of patients achieves prolonged disease control. The common anti-MM treatment targets proteasome with specific inhibitors (PI). The resulting interference with protein degradation

Dysregulated mRNA Translation in the G2019S LRRK2 and LRRK2 Knock-Out Mouse Brains.

Jungwoo Wren Kim et al.

eNeuro, 8(6) (2021-11-12)

The G2019S mutation in leucine-rich repeat kinase 2 (LRRK2) causes familial Parkinson's disease (PD) and is also found in a subset of idiopathic cases. Prior studies in Drosophila and human induced pluripotent stem cell (iPSC)-derived dopamine neurons uncovered a pronounced

Targeting genotoxic and proteotoxic stress-response pathways in human prostate cancer by clinically available PARP inhibitors, vorinostat and disulfiram.

Dusana Majera et al.

The Prostate, 79(4), 352-362 (2018-12-01)

Castration-resistant prostate cancer (PCa) represents a serious health challenge. Based on mechanistically-supported rationale we explored new therapeutic options based on clinically available drugs with anticancer effects, including inhibitors of PARP1 enzyme (PARPi), and histone deacetylases (vorinostat), respectively, and disulfiram (DSF

Therapeutic targeting of oxygen-sensing prolyl hydroxylases abrogates ATF4-dependent neuronal death and improves outcomes after brain hemorrhage in several rodent models.

Saravanan S Karuppagounder et al.

Science translational medicine, 8(328), 328ra29-328ra29 (2016-03-05)

Disability or death due to intracerebral hemorrhage (ICH) is attributed to blood lysis, liberation of iron, and consequent oxidative stress. Iron chelators bind to free iron and prevent neuronal death induced by oxidative stress and disability due to ICH, but

Alcohol-abuse drug disulfiram targets cancer via p97 segregase adaptor NPL4.

Zdenek Skrott et al.

Nature, 552(7684), 194-199 (2017-12-07)

Cancer incidence is rising and this global challenge is further exacerbated by tumour resistance to available medicines. A promising approach to meet the need for improved cancer treatment is drug repurposing. Here we highlight the potential for repurposing disulfiram (also

MAPK signaling triggers transcriptional induction of cFOS during amino acid limitation of HepG2 cells.

Jixiu Shan et al.

Biochimica et biophysica acta, 1853(3), 539-548 (2014-12-20)

Amino acid (AA) deprivation in mammalian cells activates a collection of signaling cascades known as the AA response (AAR), which is characterized by transcriptional induction of stress-related genes, including FBJ murine osteosarcoma viral oncogene homolog (cFOS). The present study established

HIV Exploits Antiviral Host Innate GCN2-ATF4 Signaling for Establishing Viral Replication Early in Infection.

Guochun Jiang et al.

mBio, 8(3) (2017-05-04)

Antiviral innate host defenses against acute viral infections include suppression of host protein synthesis to restrict viral protein production. Less is known about mechanisms by which viral pathogens subvert host antiviral innate responses for establishing their replication and dissemination. We

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