scholarly journals Screening of mutations in the additional sex combs like 1, transcriptional regulator, tumor protein p53, and KRAS proto-oncogene, GTPase/NRAS proto-oncogene, GTPase genes of patients with myelodysplastic syndrome

2017 ◽  
Vol 7 (4) ◽  
pp. 343-348 ◽  
Author(s):  
Carolina Leite ◽  
Lucas Delmonico ◽  
Gilda Alves ◽  
Romario José Gomes ◽  
Mariana Rodrigues Martino ◽  
...  
Keyword(s):  
Myelodysplastic Syndrome ◽  
Transcriptional Regulator ◽  
Protein P53 ◽  
Sex Combs ◽  
Tumor Protein P53 ◽  
Additional Sex Combs

scholarly journals Fusion of the additional sex combs like 1 and teashirt zinc finger homeobox 2 genes resulting from ider(20q) aberration in a patient with myelodysplastic syndrome

2013 ◽  
Vol 164 (1) ◽  
pp. 153-155 ◽  
Author(s):  
Jana Brezinova ◽  
Iveta Sarova ◽  
Halka Buryova ◽  
Jana Markova ◽  
Sarka Ransdorfova ◽  
...  
Keyword(s):  
Myelodysplastic Syndrome ◽  
Zinc Finger ◽  
Sex Combs ◽  
Additional Sex Combs

scholarly journals Upregulation of ULK1 expression in PC-3 cells following tumor protein P53 transfection by sonoporation

2015 ◽  
Vol 11 (1) ◽  
pp. 699-704 ◽  
Author(s):  
YU WANG ◽  
YI-NI CHEN ◽  
WEI ZHANG ◽  
YU YANG ◽  
WEN-KUN BAI ◽  
...  
Keyword(s):  
Protein P53 ◽  
Tumor Protein P53

Comparison of germline mosaics of genes in the Polycomb group of Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 140 (1) ◽  
pp. 231-243 ◽  
Author(s):  
M C Soto ◽  
T B Chou ◽  
W Bender
Keyword(s):  
Drosophila Melanogaster ◽  
Target Genes ◽  
Cell Types ◽  
Mitotic Recombination ◽  
Polycomb Group ◽  
Specific Cell ◽  
Independent Functions ◽  
Sex Combs ◽  
Null Phenotype ◽  
Additional Sex Combs

Abstract The genes of the Polycomb group (PcG) repress the genes of the bithorax and Antennapedia complexes, among others. To observe a null phenotype for a PcG gene, one must remove its maternal as well as zygotic contribution to the embryo. Five members of the PcG group are compared here: Enhancer of Polycomb [E(Pc)], Additional sex combs (Asx), Posterior sex combs (Psc), Suppressor of zeste 2 [Su (z) 2] and Polycomblike (Pcl). The yeast recombinase (FLP) system was used to induce mitotic recombination in the maternal germline. Mutant embryos were analyzed by staining with antibodies against six target genes of the PcG. The loss of the maternal component leads to enhanced homeotic phenotypes and to unique patterns of misexpression. E(Pc) and Su(z) 2 mutations had only subtle effects on the target genes, even when the maternal contributions were removed. Asx and Pcl mutants show derepression of the targets only in specific cell types. Psc shows unusual effects on two of the targets, Ultrabithorax and abdominal-A. These results show that the PcG genes do not act only in a common complex or pathway; they must have some independent functions.

The Additional sex combs gene of Drosophila encodes a chromatin protein that binds to shared and unique Polycomb group sites on polytene chromosomes

Development ◽  
1998 ◽  
Vol 125 (7) ◽  
pp. 1207-1216 ◽  
Author(s):  
D.A. Sinclair ◽  
T.A. Milne ◽  
J.W. Hodgson ◽  
J. Shellard ◽  
C.A. Salinas ◽  
...  
Keyword(s):  
Target Genes ◽  
Position Effect ◽  
Polytene Chromosomes ◽  
Polycomb Group ◽  
Position Effect Variegation ◽  
Sex Combs ◽  
Effect Variegation ◽  
The Central Nervous System ◽  
Additional Sex Combs ◽  
Site Recognition

The Additional sex combs (Asx) gene of Drosophila is a member of the Polycomb group of genes, which are required for maintenance of stable repression of homeotic and other loci. Asx is unusual among the Polycomb group because: (1) one Asx allele exhibits both anterior and posterior transformations; (2) Asx mutations enhance anterior transformations of trx mutations; (3) Asx mutations exhibit segmentation phenotypes in addition to homeotic phenotypes; (4) Asx is an Enhancer of position-effect variegation and (5) Asx displays tissue-specific derepression of target genes. Asx was cloned by transposon tagging and encodes a protein of 1668 amino acids containing an unusual cysteine cluster at the carboxy terminus. The protein is ubiquitously expressed during development. We show that Asx is required in the central nervous system to regulate Ultrabithorax. ASX binds to multiple sites on polytene chromosomes, 70% of which overlap those of Polycomb, polyhomeotic and Polycomblike, and 30% of which are unique. The differences in target site recognition may account for some of the differences in Asx phenotypes relative to other members of the Polycomb group.

scholarly journals Tumor Protein p53 (TP53) Testing and Li-Fraumeni Syndrome

2013 ◽  
Vol 17 (1) ◽  
pp. 31-47 ◽  
Author(s):  
April D. Sorrell ◽  
Carin R. Espenschied ◽  
Julie O. Culver ◽  
Jeffrey N. Weitzel
Keyword(s):  
Li Fraumeni Syndrome ◽  
Protein P53 ◽  
Tumor Protein P53 ◽  
Li Fraumeni

scholarly journals Significance of tumor protein p53 mutation in cellular process and drug selection in brain lower grade (WHO grades II and III) glioma

2020 ◽  
Vol 14 (12) ◽  
pp. 1139-1150
Author(s):  
Chang-feng Guo ◽  
Yugang Zhuang ◽  
Yuanzhuo Chen ◽  
Sheng Chen ◽  
Hu Peng ◽  
...  
Keyword(s):  
Differentially Expressed Genes ◽  
Tp53 Mutation ◽  
The Cancer Genome Atlas ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
World Health ◽  
Outcome Analysis ◽  
Lower Grade ◽  
Protein P53 ◽  
Tumor Protein P53

Aim: Tumor protein p53 ( TP53) mutant is one of the most frequently mutated genes in glioma. Results: The Cancer Genome Atlas data has shown that TP53 mutation is present in 49% of lower grade (World Health Organization [WHO] grades II and III) glioma patients. Data from The Genomics of Drug Sensitivity in Cancer database showed that three drugs: (5Z)-7-oxozeaenol, dabrafenib and nutlin-3a (−), have shown more resistance in patients with TP53 mutation. We identified 1100 differentially expressed genes. Functional enrichment analysis showed that the differentially expressed genes are mainly concentrated in the transport of ionic and cancer-related pathways. The top ten hub genes were identified and an outcome analysis revealed the most critical genes related to prognosis. Conclusion: Our results identified the key genes and pathways that might provide the basic proof to improve individualized treatment in patients with glioma.

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