Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.13.3 (histidine kinase)
 2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes the identification of novel plant genes that are required to ensure co-ordinated post-embryonic development. After germination the tumorous shoot development mutants of Arabidopsis thaliana develop disorganized tumorous tissue instead of organized leaves and stems. This results in green callus-like structures, which are capable of unlimited growth in vitro on hormone-free medium. The tsd mutants are recessive and belong to three complementation groups (tsd1, tsd2, tsd3). The genes were mapped to the bottom of chromosomes 5 and 1, and the top of chromosome 3, respectively. Histological analyses showed that the tsd mutants have different developmental defects. The shoot apical meristem of tsd1 formed only rudimentary leaves and was characterized by a degenerating L1 cell layer. tsd2 mutants had reduced cell adhesion and altered cell division planes in the L2 and L3 cell layers. The tumorous tissue of tsd3 mutants originated from the base of the leaf. Cytokinin levels that are inhibitory to the growth of wild-type seedlings bring about an enhanced growth response in all the tsd mutants. The steady state transcript levels of the histidine kinase CKI1 gene and the KNAT1 and STM homeobox genes were increased in tsd mutants, while mRNA levels of cell cycle genes were not altered. We hypothesize that the TSD gene products negatively regulate cytokinin-dependent meristematic activity during vegetative development of Arabidopsis.
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PMID:Tumorous shoot development (TSD) genes are required for co-ordinated plant shoot development. 1206 Feb 28

In order to obtain a comprehensive DNA methylation signature of HER2-positive breast cancer (HER2+ breast cancer), we performed a genome-wide methylation analysis on 17 HER2+ breast cancer and compared with ten normal breast tissue samples using the Illumina Infinium HumanMethylation450 BeadChip (450K). In HER2+ breast cancer, we found altered DNA methylation in genes involved in multicellular development, differentiation and transcription. Within these genes, we observed an overrepresentation of homeobox family genes, including several genes that have not been previously reported in relation to cancer (DBX1, NKX2-6, SIX6). Other affected genes included several belonging to the PI3K and Wnt signaling pathways. Notably, HER2, AKT3, HK1, and PFKP, genes for which altered methylation has not been previously reported, were also identified in this analysis. In total, we report 69 candidate biomarker genes with maximum differential methylation in HER2+ breast cancer. External validation of gene expression in a selected group of these genes (n = 13) revealed lowered mean gene expression in HER2+ breast cancer. We analyzed DNA methylation in six top candidate genes (AKR1B1, INA, FOXC2, NEUROD1, CDKL2, IRF4) using EpiTect Methyl II Custom PCR Array and confirmed the 450K array findings. Future clinical studies focusing on these genes, as well as on homeobox-containing genes and HER2, AKT3, HK1, and PFKP, are warranted which could provide further insights into the biology of HER2+ breast cancer.
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PMID:Whole genome DNA methylation signature of HER2-positive breast cancer. 2508 41