Results 121 to 130 of about 96,770 (285)

ABL kinase‐dependent phosphorylation of SH proteins promotes their direct interaction with CRK family SH2 domains

open access: yesFEBS Letters, EarlyView.
CT10 regulator of kinase (CRK) and CRK‐Like (CRKL) are signaling adaptors driving cell adhesion, motility, differentiation, and proliferation. SH2‐domain containing (SH) proteins are enriched in YXXP motifs which when phosphorylated create preferred binding sites for CRK family SH2 domains.
Phoebe M. Cousens   +8 more
wiley   +1 more source

Three-Dimensional Models of ACE and NEP Inhibitors and Their Use in the Design of Potent Dual ACE/NEP Inhibitors

open access: yes, 2016
A composite template for angiotensin converting enzyme (ACE, EC 3.4.15.1) inhibitors and a hypothetical model of the active site of neutral endopeptidase (NEP, EC 3.4.24.11) have been constructed and used to guide the design of dual ACE/NEP inhibitors ...
Colin McMartin (2994408)   +4 more
core   +1 more source

Mixed‐class J‐domain protein scaffolds promote expanded aggregate handling and multivalent Hsp70 engagement during functional disaggregase assembly

open access: yesFEBS Letters, EarlyView.
Protein aggregates threaten proteostasis and cell health. In human cells, Hsp70–J‐domain protein‐based disaggregases remove aggregates, but how they assemble remains unclear. Our biochemical findings show that DNAJA2‐ and DNAJB1‐containing disaggregase scaffolds enhance luciferase aggregate targeting, and that Hsp70 recruitment by both J‐domain ...
Anna Szlachcic, Nadinath B. Nillegoda
wiley   +1 more source

Effect of ACE inhibitors on blood ACE activity.

open access: yes, 2014
Serum samples (1/5 dilution in PBS) from pool of 10 healthy volunteers (control) and from patient # 27 (arrowed in Fig. 1 C) were incubated with different concentration of ACE inhibitors: short –enalaprilat (A) and long –teprotide (B).
Andrew B. Nesterovitch (342866)   +10 more
core   +1 more source

Reconstructing enzyme evolution by protein engineering

open access: yesFEBS Letters, EarlyView.
Natural enzyme evolution can be retraced by protein engineering methods such as directed evolution, rational design, and ancestral sequence reconstruction. These approaches reveal how enzymes emerged from ligand‐binding scaffolds, developed varying substrate preferences, formed oligomeric complexes, adapted to environmental changes, and evolved novel ...
Lukas Drexler   +2 more
wiley   +1 more source

Identification of a Shiga toxin A‐derived peptide internalized into Gb3 receptor‐bearing cells via interaction with the Shiga toxin B subunit

open access: yesFEBS Letters, EarlyView.
The process of internalization of the Shiga toxin A subunit via formation of a complex with the Shiga toxin B subunit, which specifically binds to the Gb3 receptor. The peptide is designed to act as a carrier of drugs into cancer cells. Here, we explored the potential of peptides derived from the catalytic A subunit of Shiga toxin (STxA) to be drug ...
Giulia Opassi   +6 more
wiley   +1 more source

Moexipril and left ventricular hypertrophy

open access: yesVascular Health and Risk Management, 2007
George S Chrysant1, PK NguyenUniversity of Oklahoma, 1Director, Advanced Cardiac Imaging, INTEGRIS Heart Hospital, Oklahoma City, OK, USAAbstract: Angiotensin-converting enzyme (ACE) inhibitors today are the standard therapy of patients with myocardial ...
George S Chrysant, PK Nguyen
doaj  

ACE inhibitors and the risk of lung cancer-is there causality? [PDF]

open access: yesBr J Cancer, 2023
Strauss MH, Sipahi I, Hall AS.
europepmc   +1 more source

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

open access: yesMolecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce   +11 more
wiley   +1 more source

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