Zobrazeno 1 - 10
of 30
pro vyhledávání: '"Sunita, K."'
Autor:
Sunita K. Agarwal, Nancy D. Perrier, Rajesh V. Thakker, Gerlof D. Valk, Maria Luisa Brandi, Kate E Lines
Publikováno v:
Endocr Rev
Multiple endocrine neoplasia type 1 (MEN1), a rare tumor syndrome that is inherited in an autosomal dominant pattern, is continuing to raise great interest for endocrinology, gastroenterology, surgery, radiology, genetics, and molecular biology speci
Autor:
Maya Elena Lee, Sunita K. Agarwal, Adel Mandl, Lee S. Weinstein, Jaydira Del Rivero, Jenny E Blau, Aisha Tepede
Publikováno v:
Journal of Molecular Endocrinology. 65:R1-R17
Gastroenteropancreatic neuroendocrine tumors (GEP NETs) comprise a heterogenous and diverse group of neoplasms arising from a common neuroendocrine cell origin. The majority of these tumors occur sporadically while ~20% manifest within the context of
Autor:
Sucharitha Iyer, Sunita K. Agarwal
Publikováno v:
Journal of Molecular Endocrinology. 61:R13-R24
Epigenetic regulation is emerging as a key feature in the molecular characteristics of various human diseases. Epigenetic aberrations can occur from mutations in genes associated with epigenetic regulation, improper deposition, removal or reading of
Publikováno v:
Endocrinology
The insulin-secreting pancreatic neuroendocrine tumors, insulinomas, characterized by increased pancreatic islet β-cell proliferation, express the phosphorylated isoform of the β-cell differentiation factor HLXB9 that interacts with NONO/p54NRB, a
The long noncoding RNA (lncRNA) MEG3 is significantly downregulated in pancreatic neuroendocrine tumors (PNETs). MEG3 loss corresponds with aberrant upregulation of the oncogenic hepatocyte growth factor (HGF) receptor c-MET in PNETs. Meg3 overexpres
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e89a1a09b4cd0f6de30b4c11c888ea06
https://europepmc.org/articles/PMC5660463/
https://europepmc.org/articles/PMC5660463/
Publikováno v:
Journal of Biological Chemistry. 289:5386-5398
Insulinomas (pancreatic islet β cell tumors) are the most common type of functioning pancreatic neuroendocrine tumors that occur sporadically or as a part of the MEN1 syndrome that is caused by germ line mutations in MEN1. Tissue-specific tumor pred
Pancreatic islet β-cells that lack the MEN1-encoded protein menin develop into tumors. Such tumors express the phosphorylated isoform of the β-cell differentiation transcription factor HLXB9. It is not known how phospho-HLXB9 acts as an oncogenic f
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::36698ff017ae566622dbab1ac117e566
https://europepmc.org/articles/PMC4646204/
https://europepmc.org/articles/PMC4646204/
Autor:
Sunita K. Kulkarni, Sheena E. Radford, Dimitris Masselos, Michael Carey, Carol V. Robinson, Alison E. Ashcroft
Publikováno v:
Web of Science
The refolding of four disulfide lysozyme (at pH 5.2, 20 degrees C) involves parallel pathways, which have been proposed to merge at a near-native state. This species contains stable structure in the alpha- and beta-domains but lacks a functional acti
Autor:
Nijaguna B. Prasad, Abdel G. Elkahloun, Rui Zhu Zhang, Francis S. Collins, Settara C. Chandrasekharappa, Sukhbir Kaur, Elizabeth A. Novotny, Youngmi Ji, Yi Chen, Sunita K. Agarwal, Stephen J. Marx, Mon-Li Chu
Publikováno v:
Molecular Cancer Research. 5:1041-1051
Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant familial cancer syndrome characterized primarily by endocrine tumors of the parathyroids, anterior pituitary, and enteropancreatic endocrine tissues. Affected individuals carry a ger
Biallelic inactivation of MEN1 encoding menin in pancreatic neuroendocrine tumors (PNETs) associated with the multiple endocrine neoplasia type 1 (MEN1) syndrome is well established, but how menin loss/inactivation initiates tumorigenesis is not well
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d54d936036c9854d8bdd1b8143fd4415
https://europepmc.org/articles/PMC4318878/
https://europepmc.org/articles/PMC4318878/