Search Results - "Haltiwanger, Robert S."
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Deciphering the Fringe-Mediated Notch Code: Identification of Activating and Inhibiting Sites Allowing Discrimination between Ligands
Published in Developmental cell (23-01-2017)“…Fringe proteins are β3-N-acetylglucosaminyltransferases that modulate Notch activity by modifying O-fucose residues on epidermal growth factor-like (EGF)…”
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Protein O-fucosylation: structure and function
Published in Current opinion in structural biology (01-06-2019)“…•Protein O-fucosyltransferases 1 and 2 (POFUT1 and POFUT2) are ER-localized and modify EGF repeats and TSRs.•Both POFUT1 and POFUT2 are exquisitely selective…”
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Significance of glycosylation in Notch signaling
Published in Biochemical and biophysical research communications (17-10-2014)“…•Notch signaling is regulated by glycosylation of its extracellular domain.•Multiple O-linked carbohydrate modifications are found on the epidermal growth…”
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Notch-Jagged complex structure implicates a catch bond in tuning ligand sensitivity
Published in Science (American Association for the Advancement of Science) (24-03-2017)“…Notch receptor activation initiates cell fate decisions and is distinctive in its reliance on mechanical force and protein glycosylation. The…”
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Canonical Notch ligands and Fringes have distinct effects on NOTCH1 and NOTCH2
Published in The Journal of biological chemistry (23-10-2020)“…Notch signaling is a cellular pathway regulating cell-fate determination and adult tissue homeostasis. Little is known about how canonical Notch ligands or…”
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O-Glycosylation modulates the stability of epidermal growth factor-like repeats and thereby regulates Notch trafficking
Published in The Journal of biological chemistry (22-09-2017)“…Glycosylation in the endoplasmic reticulum (ER) is closely associated with protein folding and quality control. We recently described a non-canonical ER…”
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Regulation of Notch Function by O-Glycosylation
Published in Advances in experimental medicine and biology (01-01-2018)“…The Notch receptor initiates a unique intercellular signaling pathway that is evolutionarily conserved across all metazoans and contributes to the development…”
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Fringe benefits: Functional and structural impacts of O-glycosylation on the extracellular domain of Notch receptors
Published in Current opinion in structural biology (01-10-2011)“…► Notch is modified at multiple sites with O-fucose and O-glucose glycans ► Elongation of O-fucose glycans by Fringe regulates Notch-ligand binding. ► Rumi…”
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Peters Plus Syndrome Mutations Disrupt a Noncanonical ER Quality-Control Mechanism
Published in Current biology (02-02-2015)“…O-fucose is added to cysteine-rich domains called thrombospondin type 1 repeats (TSRs) by protein O-fucosyltransferase 2 (POFUT2) and is elongated with glucose…”
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Mapping Sites of O-Glycosylation and Fringe Elongation on Drosophila Notch
Published in The Journal of biological chemistry (29-07-2016)“…Glycosylation of the Notch receptor is essential for its activity and serves as an important modulator of signaling. Three major forms of O-glycosylation are…”
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ROLE OF GLYCOSYLATION IN DEVELOPMENT
Published in Annual review of biochemistry (2004)“…Researchers have long predicted that complex carbohydrates on cell surfaces would play important roles in developmental processes because of the observation…”
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Jagged1 heterozygosity in mice results in a congenital cholangiopathy which is reversed by concomitant deletion of one copy of Poglut1 (Rumi)
Published in Hepatology (Baltimore, Md.) (01-02-2016)“…Haploinsufficiency for the Notch ligand JAG1 in humans results in an autosomal‐dominant, multisystem disorder known as Alagille syndrome, which is…”
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Notch-modifying xylosyltransferase structures support an SNi-like retaining mechanism
Published in Nature chemical biology (01-11-2015)“…Structural and biochemical investigations of a xylosyltransferase in complex with a domain from its substrate Notch inform on the catalytic mechanism and the…”
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Functional characterization of zebrafish orthologs of the human Beta 3-Glucosyltransferase B3GLCT gene mutated in Peters Plus Syndrome
Published in PloS one (19-09-2017)“…Peters Plus Syndrome (PPS) is a rare autosomal recessive disease characterized by ocular defects, short stature, brachydactyly, characteristic facial features,…”
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Glycosylation of Specific Notch EGF Repeats by O-Fut1 and Fringe Regulates Notch Signaling in Drosophila
Published in Cell reports (Cambridge) (12-11-2019)“…Fringe glycosyltransferases differentially modulate the binding of Notch receptors to Delta/DLL versus Serrate/Jagged ligands by adding GlcNAc to O-linked…”
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Fringe-mediated extension of O-linked fucose in the ligand-binding region of Notch1 increases binding to mammalian Notch ligands
Published in Proceedings of the National Academy of Sciences - PNAS (20-05-2014)“…The Notch signaling pathway is essential for many aspects of development, cell fate determination, and tissue homeostasis. Notch signaling can be modulated by…”
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Modulation of the NOTCH1 Pathway by LUNATIC FRINGE Is Dominant over That of MANIC or RADICAL FRINGE
Published in Molecules (Basel, Switzerland) (30-09-2021)“…Fringes are glycosyltransferases that transfer a GlcNAc to -fucose residues on Epidermal Growth Factor-like (EGF) repeats. Three Fringes exist in mammals:…”
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Inhibition of Delta-induced Notch signaling using fucose analogs
Published in Nature chemical biology (01-01-2018)“…Protein O -fucosyltransferase 1 (Pofut1) regulates Notch activity by adding O -fucose residues to its extracellular domain. Fucose analogs were identified that…”
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O-Fucosylation of ADAMTSL2 is required for secretion and is impacted by geleophysic dysplasia-causing mutations
Published in The Journal of biological chemistry (13-11-2020)“…ADAMTSL2 mutations cause an autosomal recessive connective tissue disorder, geleophysic dysplasia 1 (GPHYSD1), which is characterized by short stature, small…”
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Hydrocephalus in mouse B3glct mutants is likely caused by defects in multiple B3GLCT substrates in ependymal cells and subcommissural organ
Published in Glycobiology (Oxford) (09-09-2021)“…Abstract Peters plus syndrome, characterized by defects in eye and skeletal development with isolated cases of ventriculomegaly/hydrocephalus, is caused by…”
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