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Katie Marchbank

Researcher at King's College London

Publications -  6
Citations -  4540

Katie Marchbank is an academic researcher from King's College London. The author has contributed to research in topics: Ubiquitin & Bone remodeling. The author has an hindex of 5, co-authored 5 publications receiving 3628 citations.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Interactions with LC3 and polyubiquitin chains link nbr1 to autophagic protein turnover.

TL;DR: MINT‐7034220: NBR1 physically interacts with ube2o (uniprotkb:Q6ZPJ3) by two hybrid by two hybrids.
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Neighbor of Brca1 gene (Nbr1) functions as a negative regulator of postnatal osteoblastic bone formation and p38 MAPK activity

TL;DR: It is shown that genetic truncation of murine Nbr1 leads to an age-dependent increase in bone mass and bone mineral density through increased osteoblast differentiation and activity and pharmacological inhibition of the p38 MAPK pathway in vitro abrogates the increased osteOBlast differentiation of N br1tr/tr cells.
Journal ArticleDOI

MAP1B Interaction with the FW Domain of the Autophagic Receptor Nbr1 Facilitates Its Association to the Microtubule Network.

TL;DR: This study demonstrates an interaction between the evolutionarily conserved FW domain of Nbr1 with the microtubule-associated protein MAP1B, the first evidence that links the ubiquitin receptor NBR1, which shuttles ubiquitinated proteins to be degraded by autophagy, to the micro Tubule network.
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Autophagic receptors Nbr1 and p62 coregulate skeletal remodeling

TL;DR: It is shown that truncation of Nbr1 in a murine model, where it can still interact with p62 but not LC3, leads to increased osteoblast differentiation and activity in vivo, which results in an age-dependent increase in bone mass and bone mineral density.