Browse our anti-Ret Proto-Oncogene (RET) Antibodies

Zebrafish Ret Proto-Oncogene (RET) interaction partners

1. Authors observed no interaction between efn-A5b and RET from zebrafish, this lack of association indicates how complex efn-A signaling is and suggests that there may be other molecules involved in efn-A5-induced RET signaling.

2. These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.

3. Significantly, we show that introduction of mapk10 mutations into ret heterozygotes enhanced the ENS deficit, supporting MAPK10 as a Hirschsprung disease (HSCR) susceptibility locus. Our studies demonstrate that ret heterozygous zebrafish is a sensitized model, with many significant advantages over existing murine models, to explore the pathophysiology and complex genetics of HSCR.

4. RET expression is investigated within the brain of zebrafish; both RET protein and mRNA are observed.

5. In animals lacking Ret or Gfra3 function, myogenic gene expression is reduced in forming opercular muscles, but not in non-opercular muscles derived from the same muscle anlagen.

6. evaluation of noncoding sequences at the zebrafish ret locus conserved among teleosts, and at the human RET locus, conserved among mammals

7. genes beyond RET may be implicated in the genesis of sporadic cases of HD

Human Ret Proto-Oncogene (RET) interaction partners

1. Study demonstrated that COPB2 was highly expressed in human gastric cancer cell lines, and knockdown suppressed colony formation and promoted cell apoptosis via inhibiting the RTK signaling and its downstream signaling cascade molecules.

2. Mice expressing RET(C618F) display mild C cell hyperplasia and increased numbers of enteric neurons, indicating that RET(C618F) confers gain-of-function phenotypes. This mouse line serves as a novel biological platform for investigating pathogenetic mechanisms involved in MTC and enteric hyperganglionosis

3. RET-mTORC1 signaling promotes AML through autophagy suppression.

4. When grouped by mutational risk (highest; high; moderate-high; low-moderate; polymorphism), the age-related progression of MTC was significant for all four categories of RET mutations, which differed significantly across and within the three histopathological groups.

5. We emphasize that novel approaches to targeting RET-dependent tumours are necessary to improve the clinical efficacy of single-agent multikinase inhibition and, thus, hasten approvals of RET-directed targeted therapies

6. results affirmed that RET mutation is a reliable molecular biomarker to identify a group of highly aggressive sporadic medullary thyroid carcinoma (meta-analysis)

7. We confirmed the co-expression of RET and ER, but we did not find RET expression to be an independent prognostic factor in human breast cancer

8. Combinations of rare variants and the common non-coding RET variant cause the majority of the Hirschsprung disease cases in the studied population.

9. Report occurrence of RET gene rearangements in intraductal carcinomas of salivary gland.

10. Report molecular analysis of a group of mammary analog secretory carcinomas harboring a novel ETV6-RET translocation.

11. The role of tumor microenvironment, inflammation and NF-kappaB and RET genes expression regulation in the initiation and development of papillary thyroid carcinoma was shown. (Review)

12. A new RET gene mutation was identified causing Hirschsprung disease in an induced pluripotent cell line from a patient carrying the RET mutation.

13. we analyzed an apparently sporadic medullary thyroid carcinoma harboring a somatic RET c.1900T>C mutation [p.Cys634Arg] in a previously healthy 29-year-old man. NGS data showed that the synonymous substitution was in cis with the somatic RET p.Cys634Arg driver mutation, and subsequent experiments demonstrated that it exerted appreciable effects on RET pre-mRNA splicing.

14. we detected RET gene rearrangements in 384 patients with advanced primary NSCLC by RT-PCR and found a RET gene rearrangement rate of 1.82%. We also found a higher prevalence of RET gene rearrangements in primary compared with metastatic lesions (chi2=91.117, P<0.001). The presence of RET rearrangement in the primary tumor could be predicted by rearrangement in the corresponding metastatic lesion (kappa=0.798, P<0.001)

15. mutation was found in 23.8% of hereditary medullary thyroid carcinoma patients tested; most commonly mutated codon was codon 634 (37.1%), followed by codon 918 (14.3%)

16. Novel low frequency SNP in ERT locus is associated with Hirschsprung disease.

17. RET alterations, such as RET-oncogene fusions, are present in a subset of breast cancers, and are promising therapeutic targets.

18. RET gene alterations (copy number gain and rearrangement) exist in all RET-positive samples. RET-positive expression is a relatively independent factor in non-small cell lung cancer cases(NSCLC) patients, which indicates that the RET gene may be a novel target site for personalized treatment of NSCLC.

19. Somatic mutations of the RET gene are underrecognized in HSCR. Molecular investigation of the parents of patients with seemingly sporadic mutations is essential to determine recurrence risk in these families.

20. in vitro transactivation of the RET promoter by different Hirschsprung disease-associated PHOX2B polyA variants has resulted significantly lower compared to the effect of PHOX2B wild type protein.

Mouse (Murine) Ret Proto-Oncogene (RET) interaction partners

1. Immunohistochemistry and random sparse recombination coupled with histochemical AP staining provided an in-depth characterization of retinal ganglion cells (RGCs), horizontal cells (HCs) and amacrine cells (ACs) expressing RET. Ret is expressed in at least three distinct types of ACs, and ten types of RGCs. Ret expression overlaps with Brn3a in 4 RGC types, with Brn3b in 5 RGC types, and with Brn3c in one RGC type.

2. An oncogenic role of non-mutated Ret in the mammary gland.

3. p75 is required for the development of the nonpeptidergic nociceptor lineage by fine-tuning Ret-mediated trophic support.

4. 7-DHC efficiently supports Ret signaling in vitro.

5. Results showed that Mn-mediated age-related hearing loss involved a decreased expression and phosphorylation levels of c-Ret in spiral ganglion neurons.

6. Compromised Survival of Cerebellar Molecular Layer Interneurons Lacking GDNF Receptors GFRalpha1 or RET Impairs Normal Cerebellar Motor Learning

7. Data show that NEDL2 regulates GDNF/Ret/Akt pathway depends on its Nedd8 ligase activity rather than ubiquitin ligase activity.

8. The cardiac GFRA2 signaling pathway is distinct from the canonical pathway dependent on the RET tyrosine kinase.

9. Ret is essential to mediate GDNF's neuroprotective and neuroregenerative effect in a Parkinson disease mouse model.

10. Mechanistically, Ret is engaged in a positive feedback loop with Wnt/Wingless signalling, modulated by Src and Fak kinases.

11. Authors did not find evidence for genetic interaction between Ret and Sema3d affecting survival, presence of myenteric plexus or intestine transcriptome.

12. findings uncover a novel spinal circuit that mediates crosstalk between touch and pain pathways and suggest that some early RET positive Dorsal Horn neurons could function as pain "gating" neurons.

13. Using an organ culture system for prostate development and Ret mutant mice, we demonstrate that RET-mediated GDNF signaling in UGS increases proliferation of mesenchyme cells and suppresses androgen-induced proliferation and differentiation of prostate epithelial cells, inhibiting prostate development.

14. we described a RET-ER81-Neuregulin1 signaling pathway in neurons innervating Pacinian corpuscle somatosensory end organs, which is essential for communication between the innervating axon and the end organ

15. These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.

16. Hox proteins coordinate motor neuron differentiation and connectivity programs through Ret/Gfra genes.

17. Ret and Gfra2 null mice display comparable early central projection deficits, but Gfra2 null rapidly adapting mechanoreceptors recover later.

18. Parkin and the RET signaling cascade converge to control mitochondrial integrity and thereby properly maintain substantia nigra pars compacta dopaminergic neurons and their innervation in the striatum.

19. the Ret signaling pathway is important for podocyte survival and recovery from glomerular injury in vivo

20. RET coupling to ERK and Akt depends strongly on artemin concentration, and it is highest at the low (~100 pM) artemin levels required for neurite outgrowth.