Results 81 to 90 of about 252,333 (374)
A Cubic Equation of State for Amyloid Plaque Formation [PDF]
Protein function depends on both protein structure and amino acid (aa) sequence. Here we show that modular features of both structure and function can be quantified from the aa sequence alone for the amyloid 770 aa precursor protein A4. Both the new second order hydropathicity scale, based on evolutionary optimization (self-organized criticality), and ...
arxiv
Supramolecular Gels as Active Tools for Reaction Engineering
The unique combination of environments within gels, self‐assembled from low‐molecular‐weight gelators, offers the ability to control reactivity in new ways, achieving unique reaction outcomes, leading to the emerging concept of supramolecular gels as nanoreactors. Smart chemical engineering methods enable the use of such gels to fabricate materials and
David K. Smith
wiley +2 more sources
Polyglutamine (polyQ) tract expansion (≥ 36 amino acids) within the N‐terminal region of the Huntingtin protein (Httex1) causes Huntington's disease (HD), for which the underlying causes are not well‐understood. The authors performed computer simulations to understand the cause of HD at the molecular level.
Priyesh Mohanty+2 more
wiley +1 more source
Fractal Scaling of Cortical Matter, Amyloid Fragmentation and Plaque Formation across Rodents and Primates [PDF]
Thermodynamic tools are well suited to connecting evolution of protein functionalities to mutations of amino acid sequences, especially for neuronal network structures. These tools enable one to quantify changes in modular structure and correlate them with corresponding changes in observable properties.
arxiv
Nanoparticle‐Mediated Targeted Protein Degradation: An Emerging Therapeutics Technology
Targeted protein degradation (TPD) has emerged as a powerful therapeutic approach, with numerous candidates molecules now advancing into clinical development. Recent innovations have incorporated nanoparticles to facilitate and enhance these degradation processes, yielding synergistic effects.
Andrew G. Baker+3 more
wiley +2 more sources
Amyloid beta peptide (Abeta), the principal proteinaceous component of amyloid plaques in brains of Alzheimer's disease patients, is derived by proteolytic cleavage of the amyloid precursor protein (APP).
S. Lammich+7 more
semanticscholar +1 more source
Copper Promotes the Trafficking of the Amyloid Precursor Protein [PDF]
Accumulation of the amyloid β peptide in the cortical and hippocampal regions of the brain is a major pathological feature of Alzheimer disease. Amyloid β peptide is generated from the sequential protease cleavage of the amyloid precursor protein (APP). We reported previously that copper increases the level of APP at the cell surface.
Ashley I. Bush+11 more
openaire +4 more sources
This study reveals that Testosterone–Androgen Receptor signaling delays elderly male bone destruction by upregulation of the osteoblastic extracellular tenascin‐C (TNC). The osteoprotective effect of fibrinogen C‐terminus of TNC is demonstrated in male osteoporotic mice model that osteoblast‐specific Ar‐knockout, potentially via inhibition of ...
Yong Xie+8 more
wiley +1 more source
Protein Regge Trajectories, Phase Coexistence and Physics of Alzheimer's Disease [PDF]
Alzheimer's disease causes severe neurodegeneration in the brain that leads to a certain death. The defining factor is the formation of extracellular senile amyloid plaques in the brain. However, therapeutic approaches to remove them have not been effective in humans, and so our understanding of the cause of Alzheimer's disease remains incomplete. Here
arxiv
Targeting Amyloid‐β (Aβ) aggregation requires a peptide‐based approach that accounts for the structural heterogeneity of Aβ. Here, we employ topological reprogramming via disulfide bonds to stabilize antiparallel β‐sheets within the dimeric peptide.
Dongjoon Im+5 more
wiley +2 more sources