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Author

K. Knelles

Bio: K. Knelles is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Astrocyte & ASCL1. The author has an hindex of 1, co-authored 1 publications receiving 1 citations.
Topics: Astrocyte, ASCL1

Papers
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Journal ArticleDOI
TL;DR: In this article, the authors examined the transcriptome induced by the proneural factors Ascl1 and Neurog2 in spinal cord-derived astrocytes in vitro.

15 citations


Cited by
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Journal ArticleDOI
01 Feb 2022-Neuron
TL;DR: In this article , the authors discuss the importance of the starter cell for shaping the outcome of neuronal reprogramming and propose a code of conduct to avoid artifacts and pitfalls, and point out next challenges for less invasive cell replacement therapies for humans.

19 citations

Journal ArticleDOI
TL;DR: In this paper , the authors optimize and validate prime-seq, an early barcoding bulk RNA-seq method, and show that it performs equivalently to TruSeq, but is four times more cost-efficient due to almost 50 times cheaper library costs.
Abstract: Cost-efficient library generation by early barcoding has been central in propelling single-cell RNA sequencing. Here, we optimize and validate prime-seq, an early barcoding bulk RNA-seq method. We show that it performs equivalently to TruSeq, a standard bulk RNA-seq method, but is fourfold more cost-efficient due to almost 50-fold cheaper library costs. We also validate a direct RNA isolation step, show that intronic reads are derived from RNA, and compare cost-efficiencies of available protocols. We conclude that prime-seq is currently one of the best options to set up an early barcoding bulk RNA-seq protocol from which many labs would profit.

16 citations

Journal ArticleDOI
TL;DR: This Spotlight synthesises key concepts emerging from recent efforts to reprogramme cellular identity in vivo and provides the perspectives on recent controversies in the field of glia-to-neuron reprogramming and identifies important gaps in the understanding that present barriers to progress.
Abstract: Cellular identity is established through complex layers of genetic regulation, forged over a developmental lifetime. An expanding molecular toolbox is allowing us to manipulate these gene regulatory networks in specific cell types in vivo. In principle, if we found the right molecular tricks, we could rewrite cell identity and harness the rich repertoire of possible cellular functions and attributes. Recent work suggests that this rewriting of cell identity is not only possible, but that newly induced cells can mitigate disease phenotypes in animal models of major human diseases. So, is the sky the limit, or do we need to keep our feet on the ground? This Spotlight synthesises key concepts emerging from recent efforts to reprogramme cellular identity in vivo. We provide our perspectives on recent controversies in the field of glia-to-neuron reprogramming and identify important gaps in our understanding that present barriers to progress.

9 citations

Journal ArticleDOI
TL;DR: Findings suggest that PTB knockdown may be a promising therapeutic strategy to promote motor function recovery during spinal cord repair.

5 citations

Journal ArticleDOI
TL;DR: Evidence is brought together from different areas of neuroscience—such as neurological disorders, adult‐brain neurogenesis, innate behaviours, cell grafting, and in vivo cell reprogramming—which demonstrates robust circuit formation in adult brain, highlighting that the adult brain has higher capacity for structural plasticity than previously recognized.
Abstract: Neurons in the mammalian central nervous system display an enormous capacity for circuit formation during development but not later in life. In principle, new circuits could be also formed in adult brain, but the absence of the developmental milieu and the presence of growth inhibition and hundreds of working circuits are generally viewed as unsupportive for such a process. Here, we bring together evidence from different areas of neuroscience—such as neurological disorders, adult‐brain neurogenesis, innate behaviours, cell grafting, and in vivo cell reprogramming—which demonstrates robust circuit formation in adult brain. In some cases, adult‐brain rewiring is ongoing and required for certain types of behaviour and memory, while other cases show significant promise for brain repair in disease models. Together, these examples highlight that the adult brain has higher capacity for structural plasticity than previously recognized. Understanding the underlying mechanisms behind this retained plasticity has the potential to advance basic knowledge regarding the molecular organization of synaptic circuits and could herald a new era of neural circuit engineering for therapeutic repair.

4 citations