Results 151 to 160 of about 1,367,723 (286)

Pharmacological inhibition of the PERK pathway modulates hepatocellular carcinoma growth and immune signaling

open access: yesFEBS Open Bio, EarlyView.
Pharmacological inhibition of PERK in a DEN‐induced mouse model of liver cancer does not reduce tumor burden but alters cellular stress signaling. Despite blocking PERK activity, downstream stress responses, including CHOP expression, remain active, suggesting compensatory mechanisms within the unfolded protein response that may influence tumor ...
Ada Lerma‐Clavero   +5 more
wiley   +1 more source

Natural Products as Geroprotective Modulators in Diabetic Nephropathy: A Mechanistic Framework Integrating Aging Hallmarks and the AMPK–SIRT1–Nrf2 Axis

open access: yesAging and Cancer, EarlyView.
Natural products target the aging kidney in diabetic nephropathy by restoring the AMPK–SIRT1–Nrf2 axis, reducing oxidative stress, inflammation, fibrosis, and cellular senescence while enhancing mitochondrial biogenesis and antioxidant defenses.
Sherif Hamidu   +8 more
wiley   +1 more source

Increased brightness of fluorescent uridine, qU, inside single- and double-stranded RNA. [PDF]

open access: yesSci Rep
Karlsson AFE   +5 more
europepmc   +1 more source

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

Matrix characterization of oscillation for double sequences

open access: yesOpen Mathematics, 2008
Patterson Richard   +2 more
doaj   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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