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Annika Budnik

Researcher at University of Bristol

Publications -  6
Citations -  542

Annika Budnik is an academic researcher from University of Bristol. The author has contributed to research in topics: Endoplasmic reticulum & COPII. The author has an hindex of 6, co-authored 6 publications receiving 471 citations. Previous affiliations of Annika Budnik include German Cancer Research Center.

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Journal ArticleDOI

ER exit sites – Localization and control of COPII vesicle formation

TL;DR: Parts of the formation and maintenance of these sites, the mechanisms by which cargo becomes segregated within them, and the propagation of ER exit sites (ERES) during cell division are discussed, underlining the importance of ERES to Golgi function and more widely in terms of intracellular organization and cellular function.
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Organisation of human ER-exit sites: requirements for the localisation of Sec16 to transitional ER

TL;DR: It is shown that in human cells at steady state, Sec16 localises to cup-like structures of tER that are spatially distinct from the localisation of other COPII coat components, which is consistent with a model where Sec16 acts as a platform for COPII assembly at ERES.
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The Orphan Receptor Tie1 Controls Angiogenesis and Vascular Remodeling by Differentially Regulating Tie2 in Tip and Stalk Cells.

TL;DR: It is shown that Tie1 does not function independently but exerts context-dependent effects on the related receptor Tie2, which supports an interactive model of Tie1 and Tie2 function, in which dynamically regulated Tie1 versus Tie2 expression determines the net positive or negative effect of Tie2 signaling.
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TFG Promotes Organization of Transitional ER and Efficient Collagen Secretion

TL;DR: It is shown that TFG organizes transitional ER (tER) and ER exit sites (ERESs) into larger structures and suggests a key relationship between the structure and function of ERESs and a central role for TFG in optimizing COPII assembly for procollagen export.
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Characteristic phenotypes associated with congenital dyserythropoietic anemia (type II) manifest at different stages of erythropoiesis

TL;DR: It is proposed that SEC23A is able to compensate for the absence of SEC23B in mouse erythroblasts, providing a basis for the disappearance of phenotype within the erythroid lineage of a recently described SEC23 B knockout mouse.