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

Expression and purification of the extracellular domain of wild-type humanRET and the dimeric oncogenic mutant C634R.

International journal of biological macromolecules - 1 Dec 2020

Liu Yixin, Ribeiro Orquidea De Castro, Robinson James, Goldman Adrian

Abstract excerpt

The receptor tyrosine kinase RET is essential in a variety of cellular processes. RET gain-of-function is strongly associated with several cancers, notably multiple endocrine neoplasia type 2A (MEN 2A), while RET loss-of-function causes Hirschsprung's disease and Parkinson's disease. To investigate the activation mechanism of RET as well as to enable drug development, over-expressed recombinant protein is needed...

Read the complete abstract on PubMed

Topics

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

Share to Carcinogenesis
Share to Cysteine

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Disulfides

Share to Hirschsprung Disease

Share to Mammals

Share to Multiple Endocrine Neoplasia Type 2a

Share to Protein Domains

Share to Proto-Oncogene Proteins c-ret

Source

Identifiers

PMID: 32777409
DOI: 10.1016/j.ijbiomac.2020.07.290

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Expression and purification of the extracellular domain of wild-type humanRET and the dimeric oncogenic mutant C634R.PMID 32777409Read ↗

Structure and function of RET in multiple endocrine neoplasia type 2.Semantic proximity Read ↗

Self-association of the transmembrane domain of RET underlies oncogenic activation by MEN2A mutations.Semantic proximity Read ↗

Systematic structure-based analysis of RET variants in MEN2A and Hirschsprung's disease, and the paradoxical co-occurrence of both conditions.Semantic proximity Read ↗

Mechanisms of development of multiple endocrine neoplasia type 2 and Hirschsprung's disease by ret mutations.Semantic proximity Read ↗

RET Receptor Tyrosine Kinase: Role in Neurodegeneration, Obesity, and Cancer.Semantic proximity Read ↗

Neurotrophic factor receptor RET: structure, cell biology, and inherited diseases.Semantic proximity Read ↗

Molecular mechanisms of development of multiple endocrine neoplasia 2 by RET mutations.Semantic proximity Read ↗

The oncogenic CCDC6-RET fusion product is a dual ATP and ADP-dependent kinase that functions via <i>cis</i> -phosphorylationSemantic proximity Read ↗

Intrinsic susceptibility to misfolding of a hot-spot for Hirschsprung disease mutations in the ectodomain of RET.Semantic proximity Read ↗

Study of the RET receptor dysfunctions caused by mutations associated with human neoplastic disorders and developmental diseasesSemantic proximity Read ↗

Biological Effects of the Dual Phenotypic Janus Mutation of ret Cosegregating with Both Multiple Endocrine Neoplasia Type 2 and Hirschsprung’s DiseaseSemantic proximity Read ↗

RET-familial medullary thyroid carcinoma mutants Y791F and S891A activate a Src/JAK/STAT3 pathway, independent of glial cell line-derived neurotrophic factor.Semantic proximity Read ↗

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