DnaK inhibits protein synthesis in vivo and in vitro. by Carissa Chan (18310140)

Time-kill studies with 5 strains of <i>K</i>. <i>pneumoniae</i>, <i>P</i>. <i>aeruginosa</i>, <i>S</i>. <i>maltophilia</i> with concentration equal to one fold (A) or two fold (B)... by Antoine Grillon (519642)

DnaK associates with intact ribosomes and not with dismantled ribosomes. by Carissa Chan (18310140)

Predicted steady state distribution of the percent of TDLs in a 1) control animal, 2) following increased in the average residence time of lymphocytes in the lung (20 fold, from 26 seconds to 9 minutes) due to, for example, inflammation in the lung; 3) following a decreased entrance rate of TDLs into lymph nodes and Peyer's patches (20 fold, e.g., by using anti CD62L antibody); 4) following a decreased exit rate of TDLs from lymph nodes and Peyer's patches (5 fold, e.g., using FTY720). by Vitaly V. Ganusov (142019)

Trigger factor hinders DnaK-mediated reduction of protein synthesis. by Carissa Chan (18310140)

DnaK’s ATPase activity is stimulated by ribosomes and required to reduce protein synthesis. by Carissa Chan (18310140)

WCESP (2 mg/ml) decreases <i>V</i>. <i>cholerae</i> cell-surface hydrophobicity. by Daniel B. Pederson (604306)

Interpretation of HD sensitization as a change of inhibitory tone to the HD. by Abolhassan Behrouzvaziri (741985)

Preparations of DnaK protein are pure. by Carissa Chan (18310140)

Introduction of the D409V point mutation to the <i>GBA1</i> gene does not affect <i>GBA1</i> mRNA transcription or GCase protein translation. by Nicole K. Polinski (10947787)

Design, Synthesis, and Biological Evaluation of [1,2,5]Oxadiazolo[3,4‑<i>b</i>]pyridin-7-ol as Mitochondrial Uncouplers for the Treatment of Obesity and Metabolic Dysfunction-Assoc... by Mary A. Foutz (20361830)

“…In a Gubra-Amylin (GAN) mouse model of MASH, <b>SHO1122147</b> was efficacious in decreasing body weight and liver triglyceride levels at 200 mg kg^–1 day^–1 without changes in body temperature. …”

All data points from Fig 2. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 8. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 3. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 1. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 4. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 9. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 7. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

All data points from Fig 6. by Sara Hijazi (21656615)

“…Following a remyelination period of 5 weeks, PV interneuron properties were only partially recovered, suggesting that transient juvenile demyelination leads to long-lasting impairments of PV interneuron function. …”

The novel <i>carboxylesterase 1</i> variant c.662A>G may decrease the bioactivation of oseltamivir in humans by Jaeseong Oh (3947381)

“…A novel <i>CES1</i> c.662A>G single nucleotide polymorphism (SNP) was predicted to decrease CES1 enzymatic activity in an <i>in silico</i> analysis. …”