Results 161 to 170 of about 1,320,415 (233)
Evolutionary analysis across 32 placental mammals identified positive selection at residues H148 and W149 in the immune receptor FcγR1. Ancestral reconstruction combined with molecular dynamics simulations reveals how these mutations may influence receptor structure and dynamics, providing insight into the evolution of antibody recognition and immune ...
David A. Young +7 more
wiley +1 more source
SPO16 binds SHOC1 to promote homologous recombination and crossing-over in meiotic prophase I. [PDF]
Zhang Q, Ji SY, Busayavalasa K, Yu C.
europepmc +1 more source
Early‐life exposure to a high‐fat diet altered intact Achilles tendons in rat offspring, making them thinner, stiffer, and molecularly distinct even without injury. These findings suggest that developmental high‐fat diet exposure may impair tendon quality and increase susceptibility to mechanical overload or tendon injury later in life.
Heyong Yin +3 more
wiley +1 more source
Regulated Crossing-Over Requires Inactivation of Yen1/GEN1 Resolvase during Meiotic Prophase I. [PDF]
Arter M +7 more
europepmc +1 more source
Cutaneous Melanoma Drives Metabolic Changes in the Aged Bone Marrow Immune Microenvironment
Melanoma, the deadliest form of skin cancer, increasingly affects older adults. Our study reveals that melanoma induces changes in iron and lipid levels in the bone marrow, impacting immune cell populations and increasing susceptibility to ferroptosis.
Alexis E. Carey +12 more
wiley +1 more source
Variation and Evolution of the Meiotic Requirement for Crossing Over in Mammals. [PDF]
Dumont BL.
europepmc +1 more source
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
Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance
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
Roles for mismatch repair family proteins in promoting meiotic crossing over. [PDF]
Manhart CM, Alani E.
europepmc +1 more source

