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These data provide the first evidence for a physiologic role of these isoforms in RET pathway function.
Significantly, we show that introduction of mapk10 (show MAPK10 ELISA Kits) mutations into ret heterozygotes enhanced the ENS deficit, supporting MAPK10 (show MAPK10 ELISA Kits) as a Hirschsprung disease (HSCR (show EDNRB ELISA Kits)) 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 (show EDNRB ELISA Kits).
RET expression is investigated within the brain of zebrafish; both RET protein and mRNA are observed.
In animals lacking Ret or Gfra3 (show GFRA3 ELISA Kits) function, myogenic gene expression is reduced in forming opercular muscles, but not in non-opercular muscles derived from the same muscle anlagen.
evaluation of noncoding sequences at the zebrafish ret locus conserved among teleosts, and at the human RET locus, conserved among mammals
genes beyond RET may be implicated in the genesis of sporadic cases of HD
DNA mutational analysis of RET germline mutations associated with medullary thyroid carcinoma in a Druze family.
These data suggest that angiogenesis in RET mutation medullary thyroid carcinomas may be more intense and complete than that found in RETwt tumors, a feature that might increase their susceptibility to antiangiogenic therapy.
Significant genetic risk for Hirschsprung disease (HSCR (show EDNRB ELISA Kits)) was imparted by rs2435357 and rs2506030 at RET and by rs12707682 at SEMA3 in a Chinese population. No evidence was found of a genetic association between HSCR (show EDNRB ELISA Kits) and either of the NRG1 (show NRG1 ELISA Kits) SNPs rs7835688 and rs16879552, at either allele or genotype level.
Durable benefits with pemetrexed-based therapies in RET-rearranged lung cancers are comparable with ALK (show ALK ELISA Kits)- and ROS1 (show ROS1 ELISA Kits)-rearranged lung cancers. When selecting therapies for patients with RET-rearranged lung cancers, pemetrexed-containing regimens should be considered.
Data suggest that the KIAA1217-RET-fusion gene is a promising target for lung cancer treatment.
The RET M918V mutation is co-segregating in 8 familial MTC (show MT1A ELISA Kits) kindreds with validated evidence of a founder effect.
Mutational analysis in 17 cases of Medullary thyroid carcinoma, the somatic missense mutation at codon 918 of RET was found in 2 of the 17 Medullary thyroid carcinoma(MTC (show MT1A ELISA Kits))s, and one case presented MEN2 phenotype including MTC (show MT1A ELISA Kits).
study provided useful information on RET variants that should be subjected to further study
Review of RET mutations and mechanisms in medullary thyroid cancer.
The cardiac GFRA2 (show GFRA2 ELISA Kits) signaling pathway is distinct from the canonical pathway dependent on the RET tyrosine kinase (show TXK ELISA Kits).
Data show that NEDL2 regulates GDNF/Ret/Akt pathway depends on its Nedd8 ligase activity rather than ubiquitin ligase activity.
The cardiac GFRA2 (show GFRA2 ELISA Kits) signaling pathway is distinct from the canonical pathway dependent on the RET tyrosine kinase (show TYRO3 ELISA Kits).
Ret is essential to mediate GDNF's neuroprotective and neuroregenerative effect in a Parkinson disease mouse model.
Mechanistically, Ret is engaged in a positive feedback loop with Wnt/Wingless signalling, modulated by Src and Fak kinases.
Authors did not find evidence for genetic interaction between Ret and Sema3d (show SEMA3D ELISA Kits) affecting survival, presence of myenteric plexus or intestine transcriptome.
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.
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.
we described a RET-ER81 (show ETV1 ELISA Kits)-Neuregulin1 signaling pathway in neurons innervating Pacinian corpuscle somatosensory end organs, which is essential for communication between the innervating axon and the end organ
Hox (show MSH2 ELISA Kits) proteins coordinate motor neuron differentiation and connectivity programs through Ret/Gfra genes.
This gene, a member of the cadherin superfamily, encodes one of the receptor tyrosine kinases, which are cell-surface molecules that transduce signals for cell growth and differentiation. This gene plays a crucial role in neural crest development, and it can undergo oncogenic activation in vivo and in vitro by cytogenetic rearrangement. Mutations in this gene are associated with the disorders multiple endocrine neoplasia, type IIA, multiple endocrine neoplasia, type IIB, Hirschsprung disease, and medullary thyroid carcinoma. Two transcript variants encoding different isoforms have been found for this gene. Additional transcript variants have been described but their biological validity has not been confirmed.
proto-oncogene tyrosine-protein kinase receptor Ret
, receptor tyrosine kinase
, ret proto-oncogene
, proto-oncogene tyrosine-protein kinase receptor Ret-like
, RET transforming sequence
, cadherin family member 12
, cadherin-related family member 16
, hydroxyaryl-protein kinase
, proto-oncogene c-Ret
, ret proto-oncogene (multiple endocrine neoplasia and medullary thyroid carcinoma 1, Hirschsprung disease)
, Ret gene for receptor tyrosin
, Ret proto-oncogene (multiple endocrine neoplasia MEN2A MEN2B and medullary thyroid carcinoma 1 Hirschsprung disease)
, ret tyrosine kinase