Evan Yang
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Articles by Evan Yang
In situ profiling of plasma cell clonality with image-based single-cell transcriptomics
Abstract Image-based single-cell transcriptomics can identify diverse cell types in intact tissues. However, in adaptive immunity, V(D)J recombination generates unique immune receptors in cells of the same type, leading to important functional variation that is not yet defined by these methods.
GENIE: a multi-agent system for closed-loop autonomous microscopy
Abstract Microscopy is foundational to biology, enabling direct observation of otherwise inaccessible cellular structures and processes. Artificial intelligence has advanced microscopy through acquisition control, image analysis, and natural language instrument operation. No system has unified these steps into a complete experimental loop.
In situ profiling of plasma cell clonality with image-based single-cell transcriptomics
Abstract Image-based single-cell transcriptomics can identify diverse cell types within intact tissues. However, in adaptive immunity, V(D)J recombination generates unique immune receptors within cells of the same type, leading to important functional variation that is not yet defined by these methods.
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Charting the cellular biogeography in colitis reveals fibroblast trajectories and coordinated spatial remodeling
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Human and mouse activin genes: Divergent expression of activin A protein variants and identification of a novel heparan sulfate-binding domain in activin B
Loading metrics Open Access Peer-reviewed Research Article Paul C. Billings , Candice Bizzaro , Evan Yang , Juliet Chung, Christina Mundy, Maurizio Pacifici Paul C.
Identification and characterization of a novel heparan sulfate-binding domain in Activin A longest variants and implications for function
Loading metrics Open Access Peer-reviewed Research Article Evan Yang, Christina Mundy, Eric F. Rappaport, Maurizio Pacifici, Paul C. Billings Evan Yang, Christina Mundy, Eric F. Rappaport, Maurizio Pacifici, Paul C. Billings Published: September 19, 2019 https://doi.org/10.1371/journal.pone.0222784 Figures Abstract Activins regulate numerous processes including inflammation and are synthesized as precursors consisting of a long N-terminal pro-region and a mature protein.
Legendary ice climber Will Gadd helps climate scientists navigate melting glaciers
For Will Gadd, “fear and danger are constant – they remind me to pay attention,” he told “Nightline.” Interested in Climate Change? Add Climate Change as an interest to stay up to date on the latest Climate Change news, video, and analysis from ABC News. The places Gadd works in “are really hazardous,” he said. “If you are not afraid of that environment, something is wrong with you.” Where most see a remote and unforgiving landscape, Gadd sees a playground.
Domains with highest heparan sulfate-binding affinity reside at opposite ends in BMP2/4 versus BMP5/6/7: Implications for function
Signaling proteins, including bone morphogenetic proteins (BMPs), specifically interact with heparan sulfate (HS). These interactions regulate protein distribution and function and are largely mediated by domains rich in basic amino acids. The N-terminal region of BMP2 and BMP4 contains one such domain with a typical Cardin-Weintraub (CW) motif, but it is unclear whether the same occurs in BMP5, BMP6, and BMP7 that constitute a separate evolutionary subgroup.
Domains with highest heparan sulfate-binding affinity reside at opposite ends in BMP2/4 versus BMP5/6/7: Implications for function
Signaling proteins, including bone morphogenetic proteins (BMPs), specifically interact with heparan sulfate (HS). These interactions regulate protein distribution and function and are largely mediated by domains rich in basic amino acids. The N-terminal region of BMP2 and BMP4 contains one such domain with a typical Cardin-Weintraub (CW) motif, but it is unclear whether the same occurs in BMP5, BMP6 and BMP7 that constitute a separate evolutionary subgroup.
Heparan sulfate antagonism alters bone morphogenetic protein signaling and receptor dynamics, suggesting a mechanism in hereditary multiple exostoses
Hereditary multiple exostoses (HME) is a pediatric disorder caused by heparan sulfate (HS) deficiency and is characterized by growth plate–associated osteochondromas. Previously, we found that osteochondroma formation in mouse models is preceded by ectopic bone morphogenetic protein (BMP) signaling in the perichondrium, but the mechanistic relationships between BMP signaling and HS deficiency remain unclear.
Heparan sulfate antagonism alters bone morphogenetic protein signaling and receptor dynamics, suggesting a mechanism in Hereditary Multiple Exostoses
Hereditary Multiple Exostoses (HME) is a pediatric disorder caused by heparan sulfate (HS) deficiency and is characterized by growth plate-associated osteochondromas. Previously, we found that osteochondroma formation in mouse models is preceded by ectopic bone morphogenetic protein (BMP) signaling in the perichondrium, but the mechanistic relationships between BMP signaling and HS deficiency remain unclear.
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