Evaluation of semi-homogeneous assay formats for dual-specificity antibodies

2013 ◽  
Vol 387 (1-2) ◽  
pp. 51-56 ◽  
Author(s):  
Guoying Jiang ◽  
Chung W. Lee ◽  
Pin Yee Wong ◽  
Hélène Gazzano-Santoro
Keyword(s):  
Dual Specificity ◽  
Homogeneous Assay

Avances moleculares en el síndrome de Down y su posible aplicación en neurología

2015 ◽  
Vol 20 (1) ◽  
pp. 65-78
Author(s):  
Manuel Ramos-Kuri ◽  
Enrique Salgado-Sánchez
Keyword(s):  
Tyrosine Phosphorylation ◽  
Dual Specificity

Se revisan los avances recientes en el síndrome de Down (SD), haciendo énfasis en su terapia molecular y potencial terapéutico en enfermedades como Alzheimer (EA) y otros trastornos de déficit cognoscitivo. El SD es la principal causa de retraso mental a nivel mundial, causado por la trisomía completa o parcial del cromosoma 21, y es bien conocida su estrecha relación con la EA, de inicio muy temprano. La sobre-expresión de genes del cromosoma 21 es la principal causa del SD, pero se han identificado algunos genes especialmente importantes. Por ejemplo, el gen DYRK1A (dual specificity tyrosine phosphorylation-regulated kinase) participa en el déficit cognitivo tanto en SD como en la EA. Su fisiopatología es porque el exceso de DYRK1A hiper fosforila a la proteína precursora de amiliode (APP) y a la unidad asociada a tubulina (TAU) proteínas bien conocidas en la génesis de la EA. Otra aplicación potencial es que los pacientes con SD presentan menor incidencia de tumores sólidos; su mecanismo es inhibiendo angiogénesis, por inhibición del factor de crecimiento vascular endotelial (VEGF) a través de la inhibición de calcineurina, gracias a la sobre-expresión del gen DSCR-1 presente en el cromosoma 21. Aunque el SD aún no cuenta con terapia específica, se realiza terapia molecular en modelos murinos con SD, con dos péptidos intestinales vasoactivos NAP y SAL. Los ratones así tratados mostraron una clara disminución en el déficit cognoscitivo, sugiriendo un alto potencial terapéutico para el SD; así como, otros tipos de retardo mental y déficit de aprendizaje.

Study on interaction between Duodenase - Protease with Dual Specificity and Inhibitors of Bowman-Birk Family

2002 ◽  
Vol 9 (2) ◽  
pp. 139-144 ◽  
Author(s):  
Inna Gladysheva ◽  
Natalia Popykina ◽  
Tatyana Zamolodchikova ◽  
Natalia Larionova
Keyword(s):  
Dual Specificity

scholarly journals Characterization of Caenorhabditis elegans Homologs of the Down Syndrome Candidate Gene DYRK1A

Genetics ◽  
2003 ◽  
Vol 163 (2) ◽  
pp. 571-580 ◽  
Author(s):  
William B Raich ◽  
Celine Moorman ◽  
Clay O Lacefield ◽  
Jonah Lehrer ◽  
Dusan Bartsch ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Caenorhabditis Elegans ◽  
Trisomy 21 ◽  
Gene Dosage ◽  
Inducible Promoters ◽  
C Elegans ◽  
Dual Specificity ◽  
Specificity Protein

Abstract The pathology of trisomy 21/Down syndrome includes cognitive and memory deficits. Increased expression of the dual-specificity protein kinase DYRK1A kinase (DYRK1A) appears to play a significant role in the neuropathology of Down syndrome. To shed light on the cellular role of DYRK1A and related genes we identified three DYRK/minibrain-like genes in the genome sequence of Caenorhabditis elegans, termed mbk-1, mbk-2, and hpk-1. We found these genes to be widely expressed and to localize to distinct subcellular compartments. We isolated deletion alleles in all three genes and show that loss of mbk-1, the gene most closely related to DYRK1A, causes no obvious defects, while another gene, mbk-2, is essential for viability. The overexpression of DYRK1A in Down syndrome led us to examine the effects of overexpression of its C. elegans ortholog mbk-1. We found that animals containing additional copies of the mbk-1 gene display behavioral defects in chemotaxis toward volatile chemoattractants and that the extent of these defects correlates with mbk-1 gene dosage. Using tissue-specific and inducible promoters, we show that additional copies of mbk-1 can impair olfaction cell-autonomously in mature, fully differentiated neurons and that this impairment is reversible. Our results suggest that increased gene dosage of human DYRK1A in trisomy 21 may disrupt the function of fully differentiated neurons and that this disruption is reversible.

scholarly journals Dual-specificity phosphatase 3 deletion promotes obesity, non-alcoholic steatohepatitis and hepatocellular carcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sophie Jacques ◽  
Arash Arjomand ◽  
Hélène Perée ◽  
Patrick Collins ◽  
Alice Mayer ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Damage ◽  
Chow Diet ◽  
Serum Triglycerides ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Steatohepatitis ◽  
Dual Specificity ◽  
Dual Specificity Protein Phosphatase

AbstractNon-alcoholic fatty liver disease (NAFLD) is the most common chronic hepatic pathology in Western countries. It encompasses a spectrum of conditions ranging from simple steatosis to more severe and progressive non-alcoholic steatohepatitis (NASH) that can lead to hepatocellular carcinoma (HCC). Obesity and related metabolic syndrome are important risk factors for the development of NAFLD, NASH and HCC. DUSP3 is a small dual-specificity protein phosphatase with a poorly known physiological function. We investigated its role in metabolic syndrome manifestations and in HCC using a mouse knockout (KO) model. While aging, DUSP3-KO mice became obese, exhibited insulin resistance, NAFLD and associated liver damage. These phenotypes were exacerbated under high fat diet (HFD). In addition, DEN administration combined to HFD led to rapid HCC development in DUSP3-KO compared to wild type (WT) mice. DUSP3-KO mice had more serum triglycerides, cholesterol, AST and ALT compared to control WT mice under both regular chow diet (CD) and HFD. The level of fasting insulin was higher compared to WT mice, though, fasting glucose as well as glucose tolerance were normal. At the molecular level, HFD led to decreased expression of DUSP3 in WT mice. DUSP3 deletion was associated with increased and consistent phosphorylation of the insulin receptor (IR) and with higher activation of the downstream signaling pathway. In conclusion, our results support a new role for DUSP3 in obesity, insulin resistance, NAFLD and liver damage.

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