Analysis of change in mature INPs, GMCs and neurons in the type II NB lineage on depletion of mitochondrial morphology proteins. by Dnyanesh Dubal (12085942)

Demonstration of test steps. by Jin Zhu (164147)

Analysis of proliferation in NBs depleted of Opa1 and Marf. by Dnyanesh Dubal (12085942)

Depletion of Opa1 and Marf does not cause increase in the cleaved Caspase 3 levels and apoptosis in the brain. by Dnyanesh Dubal (12085942)

Notch signaling regulates fused mitochondrial morphology in INPs and muscle cells. by Dnyanesh Dubal (12085942)

Phase plot of the periodic orbits for progressive (Panel A) and alternating stepping (Panel B). by Hendrik Reimann (3778705)

Exposure to IQ3A compounds decreases <i>HSP90</i> and <i>KRAS</i> mRNA, protein expression and <i>KRAS</i> transcription. by Hugo Brito (747224)

Drp1^SD overexpression partially alleviates the differentiation defect seen in <i>notch</i> RNAi expressing type II NB lineages. by Dnyanesh Dubal (12085942)

Analysis of mitochondrial morphology in Notch mutants and Notch signaling in Opa1 depleted type II NB lineages. by Dnyanesh Dubal (12085942)

Schematic of the multi-Step model. by Anshul Saini (11320669)

Image1_Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism.TIF by Franciel Batista Felix (10699536)

“…BCA treatment shortened Ri from ∼23 h observed in vehicle-treated mice to ∼5.5 h, associated with an increase in apoptotic events and efferocytosis, both key steps for the resolution of inflammation. These effects of BCA were prevented by H89, an inhibitor of protein kinase A (PKA) and G15, a selective G protein–coupled receptor 30 (GPR30) antagonist. …”

Image2_Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism.TIF by Franciel Batista Felix (10699536)

“…BCA treatment shortened Ri from ∼23 h observed in vehicle-treated mice to ∼5.5 h, associated with an increase in apoptotic events and efferocytosis, both key steps for the resolution of inflammation. These effects of BCA were prevented by H89, an inhibitor of protein kinase A (PKA) and G15, a selective G protein–coupled receptor 30 (GPR30) antagonist. …”

Image4_Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism.TIF by Franciel Batista Felix (10699536)

“…BCA treatment shortened Ri from ∼23 h observed in vehicle-treated mice to ∼5.5 h, associated with an increase in apoptotic events and efferocytosis, both key steps for the resolution of inflammation. These effects of BCA were prevented by H89, an inhibitor of protein kinase A (PKA) and G15, a selective G protein–coupled receptor 30 (GPR30) antagonist. …”

Image3_Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism.TIF by Franciel Batista Felix (10699536)

“…BCA treatment shortened Ri from ∼23 h observed in vehicle-treated mice to ∼5.5 h, associated with an increase in apoptotic events and efferocytosis, both key steps for the resolution of inflammation. These effects of BCA were prevented by H89, an inhibitor of protein kinase A (PKA) and G15, a selective G protein–coupled receptor 30 (GPR30) antagonist. …”

Decreased oscillatory flow decreases <i>klf2a</i> expression. by Julien Vermot (257990)

“…<p>(A) RFF is decreased by alterations in heart rate. …”

Fig 4 - by Min Sub Sim (8193564)

Fig 3 - by Min Sub Sim (8193564)

Juvenile demyelination induces a loss of functional autapses. by Sara Hijazi (21656615)

“…Cuprizone-treated mice show a significant decrease in the percentage of cells showing an autaptic response (<i>Fisher’s exact test; *p = 0.0173</i>). …”

Seven out of the 11 human cytidine deaminases are more highly expressed in tumor versus normal tissue and their higher expression is correlated with a decrease in survival. by Mason A. McCool (11889842)

GluN2A(D731N) decreases channel open probability. by Kai Gao (120150)

“…The di-heteromeric mutant (2A-D731N) and tri-heteromeric receptors with two-copies of the mutant subunit (D731N/D731N) showed a prolonged inhibition rate, reflecting a decreased channel open probability. …”