Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genetic and biochemical evidence that gastrulation defects in Pofut2 mutants result from defects in ADAMTS9 secretion.

Developmental biology - 1 Aug 2016

Benz Brian A, Nandadasa Sumeda, Takeuchi Megumi, Grady Richard C, Takeuchi Hideyuki, LoPilato Rachel K, Kakuda Shinako, Somerville Robert P T, Apte Suneel S, Haltiwanger Robert S, Holdener Bernadette C

Abstract excerpt

Protein O-fucosyltransferase 2 (POFUT2) adds O-linked fucose to Thrombospondin Type 1 Repeats (TSR) in 49 potential target proteins. Nearly half the POFUT2 targets belong to the A Disintegrin and Metalloprotease with ThromboSpondin type-1 motifs (ADAMTS) or ADAMTS-like family of proteins. Both the mouse Pofut2 RST434 gene trap allele and the Adamts9 knockout were reported to result in early embryonic lethality,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amnion
Share to Body Patterning

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Embryonic Stem Cells

Share to Fucosyltransferases

Share to Gastrulation

Share to HEK293 Cells

Share to Mesoderm

Share to Mice, Knockout

Source

Open in PubMed Open full text

Identifiers

PMID: 27297885
DOI: 10.1016/j.ydbio.2016.05.038
PMCID: PMC5572823

Genes

ADAMTS9
POFUT2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetic and biochemical evidence that gastrulation defects in Pofut2 mutants result from defects in ADAMTS9 secretion.PMID 27297885Read ↗

ADAMTS9 and ADAMTS20 are differentially affected by loss of B3GLCT in mouse model of Peters plus syndromeSemantic proximity Read ↗

Variant in human POFUT1 reduces enzymatic activity and likely causes a recessive microcephaly, global developmental delay with cardiac and vascular features.Semantic proximity Read ↗

Genetic Diseases of Fucosylation: Insights from Model OrganismsSemantic proximity Read ↗

Emerging roles for ADAMTS5 during development and disease.Semantic proximity Read ↗

Notch signalling in the paraxial mesoderm is most sensitive to reduced Pofut1 levels during early mouse development.Semantic proximity Read ↗

A new Adamts9 conditional mouse allele identifies its non-redundant role in interdigital web regression.Semantic proximity Read ↗

Peters plus syndrome mutations disrupt a noncanonical ER quality-control mechanism.Semantic proximity Read ↗

VANGL2 regulates membrane trafficking of MMP14 to control cell polarity and migration.Semantic proximity Read ↗

Cooperation of two ADAMTS metalloproteases in closure of the mouse palate identifies a requirement for versican proteolysis in regulating palatal mesenchyme proliferation.Semantic proximity Read ↗

Matriptase drives early-onset intestinal failure in a mouse model of congenital tufting enteropathySemantic proximity Read ↗

Identification of a new allele of O-fucosyltransferase 1 involved in Drosophila intestinal stem cell regulation.Semantic proximity Read ↗

ADAM-TS5, ADAM-TS6, and ADAM-TS7, Novel Members of a New Family of Zinc MetalloproteasesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.