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66 items found for "Abigail R Walker"
Posts (35)
- A NanoBRET-Based H 3 R Conformational Biosensor to Study Real-Time H 3 Receptor Pharmacology in...
August 2022 A NanoBRET-Based H 3 R Conformational Biosensor to Study Real-Time H 3 Receptor Pharmacology
- Trevena Receives up to $40M in OLINVYK ex-US Royalty-Based Financing from R-Bridge Healthcare ...
April 2022 Trevena Receives up to $40M in OLINVYK ex-US Royalty-Based Financing from R-Bridge Healthcare disorders, today announced that the Company entered into a royalty-based financing with an affiliate of R-Bridge Healthcare Fund (the R-Bridge Financing)."
- 📰 GPCR Weekly News, May 13 to 19, 2024
article on Illuminating GPCR Research: FRET and BRET-Based Sensors Shed Light on Cellular Signaling Abigail Walker, Aylin Hanyaloglu, et al., for their study on Constitutive internalisation of EP2 differentially
Other Pages (31)
- Ep 96 with R. Scott Struthers
GPCR Podcast << Back to podcast list Scott Struthers R. R. Scott Struthers on the web LinkedIn Google Scholar Crinetics Radionetics Dr.
- Spliceosome mutations are associated with clinical response in a phase 1b/2 study of the PLK1 inhibitor onvansertib in combination with decitabine in relapsed or refractory acute myeloid leukemia
with decitabine (DAC) demonstrated initial safety and efficacy in patients with relapsed/refractory (R/ R) AML. The current study aimed to identify molecular predictors of response to ONV + DAC in R/R AML patients A total of 44 R/R AML patients were treated with ONV + DAC and considered evaluable for efficacy. PLK1 inhibition with ONV in combination with DAC could be a potential therapy in R/R AML patients, particularly
- Context-dependent ciliary regulation of hedgehog pathway repression in tissue morphogenesis
bifunctional GLI transcription factors generate both GLI-activators (GLI-A) and GLI-repressors (GLI-R) The formation of GLI-A/GLI-R requires cilia. , and the ankyrin repeat protein ANKMY2 that direct cAMP/protein kinase-A signaling by cilia in GLI-R GLI-A formation only, or dual regulation of either lack of GLI-R or excess GLI-A formation. complex tissue-specific GLI-effector requirements in morphogenesis and point to tissue-specific GLI-R