Hernández Gutiérrez, Salomón
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Preferred name
Hernández Gutiérrez, Salomón
Official Name
Hernández Gutiérrez, Salomón
Alternative Name
shernand
Main Affiliation
ORCID
Scopus Author ID
15739969000
Researcher ID
DVV-7932-2022

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STR data for 15 loci in a population sample from the central region of Mexico

2005 , Hernández Gutiérrez, Salomón , Hernández-Franco, Pablo , Martínez-Tripp, Sara C. , Ramos Kuri, Manuel , Rangel-Villalobos, Héctor

A Mexican population sample was obtained from the central region of the country, including five states. Two hundred and eleven individuals were PCR-typed for 15 STR loci with the AmpFι STR Identifiler PCR amplification kit (Applied Biosystems). The following autosomal markers were analyzed: D8S1179, D21S11, D7S820, CSF1PO, D19S433, vWA, TPOX, D18S51, D3S1358, TH01, D13S317, D16S539, D2S1338, D5S818, FGA and Amelogenin. Allele frequencies for each STR were estimated and compared to previous reports. Genotype distribution by locus and by two loci combination was in agreement with Hardy–Weinberg expectations for all 15 STRs. This STR system in Mexican-mestizos presented a combined probability of exclusion (PE) and discrimination (PD) longer than 99.999%.

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NF-κB signaling blockade by Bay 11-7085 during early cardiac morphogenesis induces alterations of the outflow tract in chicken heart

2006 , Hernández Gutiérrez, Salomón , García-Peláez, I. , Zentella-Dehesa, Alejandro , Ramos Kuri, Manuel , Rojas, Emilio , Hernández-Franco, Pablo , Hernández-Sánchez, Fernando

Nuclear factor κB (NF-κB) is a pleiotropic transcription factor implicated in the regulation of diverse morphologic cardiac alterations, for which the p50 and p65 subunits form the most prevalent dimeric form in the heart. NF-κB is inactivated by proteins of the IκB family, which trap it in the cytoplasm. It is not known whether NF-κB influences cardiac development. Objective: Here we investigated the role of NF-κB in regulating transcription in chicken heart morphogenesis. Specifically, we tested whether NF-κB activation is required for normal formation of the outflow tract (OFT) during a critical stage of heart development. Methods and results: We designed a reporter vector with κB binding sites for Rel family members in the promoter, upstream from the cDNA of Green Fluorescent Protein (GFP). This construct was injected directly into the developing heart of chicken embryos. NF-κB activation was subsequently inhibited by administration of the specific pharmacological agent Bay 11-7085. We found that forced NF-κB expression was associated with multiple congenital cardiac alterations of the OFT (mainly IVC, DORV and great arteries stenosis). Conclusion: These findings indicate that blockade of NF-κB induces apoptosis and is an important factor in the development of OFT during cardiogenesis. However, it remains unknown which members of the Rel family are relevant in this process. ©Apoptosis

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