نتایج جستجو برای: ret

تعداد نتایج: 4062  

Journal: :Neuron 1998
Robert H Baloh Malú G Tansey Patricia A Lampe Timothy J Fahrner Hideki Enomoto Kelli S Simburger Melanie L Leitner Toshiyuki Araki Eugene M Johnson Jeffrey Milbrandt

The glial cell line-derived neurotrophic factor (GDNF) ligands (GDNF, Neurturin [NTN], and Persephin [PSP]) signal through a multicomponent receptor system composed of a high-affinity binding component (GFRalpha1-GFRalpha4) and a common signaling component (RET). Here, we report the identification of Artemin, a novel member of the GDNF family, and demonstrate that it is the ligand for the forme...

2014
Iván Plaza-Menacho Karin Barnouin Kerry Goodman Rubén J. Martínez-Torres Annabel Borg Judith Murray-Rust Stephane Mouilleron Phillip Knowles Neil Q. McDonald

To decipher the molecular basis for RET kinase activation and oncogenic deregulation, we defined the temporal sequence of RET autophosphorylation by label-free quantitative mass spectrometry. Early autophosphorylation sites map to regions flanking the kinase domain core, while sites within the activation loop only form at later time points. Comparison with oncogenic RET kinase revealed that lat...

Journal: :Development 2010
Yutaka Honma Masako Kawano Shinichi Kohsaka Masaharu Ogawa

Establishment of connectivity between peripheral and central organs is essential for sensory processing by dorsal root ganglion (DRG) neurons. Using Ret as a marker for mechanoreceptive DRG neurons, we show that both central and peripheral projections of mechanoreceptive neurons are severely impaired in the absence of Ret. Death of DRG neurons in Ret-deficient mice can be rescued by eliminating...

Journal: :Annals of surgery 2014
Philip M Spanheimer Anthony R Cyr Matthew P Gillum George W Woodfield Ryan W Askeland Ronald J Weigel

OBJECTIVE We investigated directed therapy based on TFAP2C-regulated pathways to inform new therapeutic approaches for treatment of luminal breast cancer. BACKGROUND TFAP2C regulates the expression of genes characterizing the luminal phenotype including ESR1 and RET, but pathway cross talk and potential for distinct elements have not been characterized. METHODS Activation of extracellular s...

Journal: :Endocrinology 2014
Esther Diaz-Rodriguez Angela R Garcia-Rendueles Alejandro Ibáñez-Costa Ester Gutierrez-Pascual Montserrat Garcia-Lavandeira Alfonso Leal Miguel A Japon Alfonso Soto Eva Venegas Francisco J Tinahones Juan A Garcia-Arnes Pedro Benito Maria Angeles Galvez Luis Jimenez-Reina Ignacio Bernabeu Carlos Dieguez Raul M Luque Justo P Castaño Clara V Alvarez

Acromegaly is caused by somatotroph cell adenomas (somatotropinomas [ACROs]), which secrete GH. Human and rodent somatotroph cells express the RET receptor. In rodents, when normal somatotrophs are deprived of the RET ligand, GDNF (Glial Cell Derived Neurotrophic Factor), RET is processed intracellularly to induce overexpression of Pit1 [Transcription factor (gene : POUF1) essential for transcr...

Journal: :Journal of medical genetics 2011
Cécile Jeanpierre Guillaume Macé Mélanie Parisot Vincent Morinière Audrey Pawtowsky Marion Benabou Jelena Martinovic Jeanne Amiel Tania Attié-Bitach Anne-Lise Delezoide Philippe Loget Patricia Blanchet Dominique Gaillard Marie Gonzales Wassila Carpentier Patrick Nitschke Frédéric Tores Laurence Heidet Corinne Antignac Rémi Salomon

BACKGROUND The RET/GDNF signalling pathway plays a crucial role during development of the kidneys and the enteric nervous system. In humans, RET activating mutations cause multiple endocrine neoplasia, whereas inactivating mutations are responsible for Hirschsprung disease. RET mutations have also been reported in fetuses with renal agenesis, based on analysis of a small series of samples. OB...

Journal: :The Journal of clinical endocrinology and metabolism 2011
Hans H G Verbeek Maria M Alves Jan-Willem B de Groot Jan Osinga John T M Plukker Thera P Links Robert M W Hofstra

CONTEXT Medullary and papillary thyroid carcinoma (MTC and PTC) are two types of thyroid cancer that can originate from activating mutations or rearrangements in the RET gene. Therapeutic options are limited in recurrent disease, but because RET is a tyrosine kinase (TK) receptor involved in cellular growth and proliferation, treatment with a TK inhibitor might be promising. Several TK inhibito...

2016
Xuan Su Zhaoqu Li Caiyun He Weichao Chen Xiaoyan Fu Ankui Yang

BACKGROUND RET/PTC rearrangements have been identified as a specific genetic event in papillary thyroid cancer (PTC). We conducted this meta-analysis to identify an enriched population who were more likely to occur RET/PTC fusion genes. METHODS All relevant studies in the PubMed, Web of Science, and Embase databases were searched up to June 2015. The studies found were screened according to o...

1998
Richard R. Hardy

Em-ret mice carrying an RFP/RET fusion gene under the transcriptional control of the immunoglobulin heavy chain enhancer develop B lineage leukemias/lymphomas. We have characterized B-cell development in these mice before the onset of clinical disease to determine the steps involved in leukemogenesis. Flow cytometry reveals that the CD45R1CD431CD241BP-11 late pro–B-cell population is markedly e...

2009
Maxim M. Bespalov

1. LITERATURE REVIEW .........................................................................................1 1.1. Growth factors and neurotrophic factors ..............................................................1 1.2. GDNF family ligands ...........................................................................................5 GFLs structure and receptor complexes .......................

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