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Barbara Panning

Researcher at University of California, San Francisco

Publications -  74
Citations -  12023

Barbara Panning is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: X-inactivation & XIST. The author has an hindex of 36, co-authored 71 publications receiving 11047 citations. Previous affiliations of Barbara Panning include McMaster University & Massachusetts Institute of Technology.

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Genome-Scale CRISPR-Mediated Control of Gene Repression and Activation

TL;DR: This work identifies rules for specific targeting of transcriptional repressors (CRISPRi), typically achieving 90%-99% knockdown with minimal off-target effects, and activators to endogenous genes via endonuclease-deficient Cas9, which enable modulation of gene expression over a ∼1,000-fold range.

Genome-Scale CRISPR-Mediated Control of Gene Repression and Activation

TL;DR: In this article, the authors identify rules for specific targeting of transcriptional repressors (CRISPRi), typically achieving 90%-99% knockdown with minimal off-target effects, and activators (CRisPRa) to endogenous genes via endonuclease-deficient Cas9.
Journal ArticleDOI

IRE1 Signaling Affects Cell Fate During the Unfolded Protein Response

TL;DR: There is a causal link between the duration of UPR branch signaling and life or death cell fate after ER stress, and key findings from studies in cell culture were recapitulated in photoreceptors expressing mutant rhodopsin in animal models of retinitis pigmentosa.
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Role of histone H3 lysine 27 methylation in X inactivation.

TL;DR: It is demonstrated that transient recruitment of the Eed-Ezh2 complex to the inactive X chromosome (Xi) occurs during initiation of X inactivation in both extraembryonic and embryonic cells and is accompanied by H3-K27 methylation.
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Xist-deficient mice are defective in dosage compensation but not spermatogenesis.

TL;DR: The results indicate that the Xist RNA is required for female dosage compensation but plays no role in spermatogenesis.