Micro-RNA regulation of the angiogenic response in the diabetic retina

Author(s):  
H.C. Campos-Borges ◽  
S.M. Sanz-González ◽  
V. Zanón-Moreno ◽  
J.M. Millán Salvador ◽  
M.D. Pinazo-Duran
2019 ◽  
Vol 97 (2) ◽  
pp. 112-122 ◽  
Author(s):  
Oliver Bruhn ◽  
Marie Lindsay ◽  
Friederike Wiebel ◽  
Meike Kaehler ◽  
Inga Nagel ◽  
...  

2009 ◽  
Vol 126 ◽  
pp. S54
Author(s):  
Catriona Alexander ◽  
David Sester ◽  
David Hume ◽  
Michael Clinton

2005 ◽  
Vol 25 (21) ◽  
pp. 9198-9208 ◽  
Author(s):  
Ligang Wu ◽  
Joel G. Belasco

ABSTRACT Vertebrate genomes each encode hundreds of micro-RNAs (miRNAs), yet for few of these miRNAs is there empirical evidence as to which mRNA(s) they regulate. Here we report the identification of human lin-28 mRNA as a regulatory target of human miR-125b and its homolog miR-125a. Studies of miR-125b function in mouse P19 embryonal carcinoma cells induced to develop into neurons suggest a role for this regulatory miRNA in mammalian neuronal differentiation, since its increased concentration in these cells contributes to lin-28 downregulation. Within the lin-28 3′ untranslated region (UTR) are two conserved miRNA responsive elements (miREs) that mediate repression by miR-125b and miR-125a. Simultaneous deletion of both miREs renders the lin-28 3′ UTR almost completely insensitive to these miRNAs, indicating that these two miREs are the principal elements in the lin-28 3′ UTR that respond to miR-125. At the 3′ end of each element is an adenosine residue that makes a significant contribution to function irrespective of its complementarity to the 5′-terminal nucleotide of miR-125. By contrast to most earlier reports of gene repression by other miRNAs that are imperfectly complementary to their targets, lin-28 downregulation by miR-125 involves reductions in both translational efficiency and mRNA abundance. The decrease in the mRNA concentration is achieved by a posttranscriptional mechanism that is independent of the inhibitory effect on translation.


2018 ◽  
Vol 25 (3) ◽  
pp. 160-165
Author(s):  
Mohammad Rasoul Samandari-Bahraseman ◽  
Mehrdad Jahanshahi ◽  
Sara Asadi Barbariha ◽  
Leila Elyasi

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Diana Drago-García ◽  
Jesús Espinal-Enríquez ◽  
Enrique Hernández-Lemus

2020 ◽  
Author(s):  
Abhijeet Gummadavelli ◽  
Lily McCarthy ◽  
Zeynep Erson ◽  
Eugenia Vining ◽  
Murat Gunel ◽  
...  
Keyword(s):  

2007 ◽  
Vol 32 (05) ◽  
Author(s):  
S Lehmann ◽  
K Gorzelniak ◽  
J Janke ◽  
S Engeli ◽  
FC Luft ◽  
...  
Keyword(s):  

2017 ◽  
Vol 26 (2) ◽  
pp. 157-163 ◽  
Author(s):  
Lakshmi Manogna Chintalacheruvu ◽  
Trudy Shaw ◽  
Avanija Buddam ◽  
Osama Diab ◽  
Thamer Kassim ◽  
...  

Gastrointestinal cancer is one of the major causes of death worldwide. Hereditary gastrointestinal cancer syndromes constitute about 5-10% of all cancers. About 20-25% of undiagnosed cases have a possible hereditary component, which is not yet established. In the last few decades, the advance in genomics has led to the discovery of multiple cancer predisposition genes in gastrointestinal cancer. Physicians should be aware of these syndromes to identify high-risk patients and offer genetic testing to prevent cancer death. In this review, we describe clinical manifestations, genetic testing and its challenges, diagnosis and management of the major hereditary gastrointestinal cancer syndromes.Key words:  −  −  −  − .Abbreviations: ACG: American College of Gastroenterology; AFAP: attenuated FAP; APC: adenomatous polyposis coli; CDH1: E-cadherin; CHRPE: congenital hypertrophy of the retinal pigment epithelium; CRC: colorectal cancer; FAMMM: Familial atypical multiple mole melanoma; FAP: Familial adenomatous polyposis; GC: gastric cancer; HDGC: Hereditary diffuse gastric cancer; IHC: immunohistochemical; IPAA: ileal pouch–anal anastomosis; IRA: ileorectal anastomosis; MSI: microsatellite instability; MMR: mismatch repair; miRNA: micro RNA.


Sign in / Sign up

Export Citation Format

Share Document