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Michal Jarnik

Researcher at National Institutes of Health

Publications -  36
Citations -  1962

Michal Jarnik is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Loricrin & Synapse. The author has an hindex of 19, co-authored 33 publications receiving 1574 citations. Previous affiliations of Michal Jarnik include Fox Chase Cancer Center.

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Lessons from Loricrin-Deficient Mice: Compensatory Mechanisms Maintaining Skin Barrier Function in the Absence of a Major Cornified Envelope Protein

TL;DR: At least one of the compensatory mechanisms preventing a more severe skin phenotype in newborn Lor−/− mice is an increase in the expression of other CE components, such as SPRRP2D and SPR RP2H, members of the family of “small proline rich proteins”, and repetin, a member of the “fused gene” subgroup of the S100 gene family.
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BORC, a Multisubunit Complex that Regulates Lysosome Positioning

TL;DR: The identification of a multisubunit complex named BORC that regulates lysosome positioning is reported, which comprises eight subunits that functions to recruit the small GTPase Arl8 and promotes the kinesin-dependent movement of lysOSomes toward the plus ends of microtubules in the peripheral cytoplasm.
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Distribution of ESCRT Machinery at HIV Assembly Sites Reveals Virus Scaffolding of ESCRT Subunits

TL;DR: The findings suggest that the ESCRT machinery required for the scission of HIV particles from infected cells is located within the core of the virus particle and not, as might have been expected based on previous work, on the cellular side of the membrane scission event involved in viral budding.
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Ama1p is a meiosis-specific regulator of the anaphase promoting complex/cyclosome in yeast

TL;DR: The requirement of Ama1p only for meiosis I and spore morphogenesis suggests a function for APC/C(Ama1) specifically adapted to germ cell development.
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Noncanonical autophagy at ER exit sites regulates procollagen turnover.

TL;DR: Overall, the findings reveal that a subset of procollagen molecules is directed toward lysosomal degradation through an autophagic pathway originating at ERESs, providing a mechanism to remove excess Procollagen from cells.