HKR1 Blocking Peptide
- Known as:
- HKR1 Blocking Peptide
- Catalog number:
- 33r-3619
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HKR1 Blocking Peptide
Related genes to: HKR1 Blocking Peptide
- Gene:
- ZNF875 NIH gene
- Name:
- zinc finger protein 875
- Previous symbol:
- HKR1
- Synonyms:
- -
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-29
- Date modifiied:
- 2019-01-22
Related products to: HKR1 Blocking Peptide
Related articles to: HKR1 Blocking Peptide
- Although an increasing number of common variants contributing to Alzheimer's disease (AD) are uncovered by genome-wide association studies, they can only explain less than half of the heritability of AD. Rare variant association studies (RVAS) has become an increasingly important area to explain the risk or trait variability of AD. - Source: PubMed
Publication date: 2022/05/07
Xiong WeixueCai JiahuiLi RuijiaWen CanhongTan HaizhuOn Behalf Of The Alzheimer's Disease Neuroimaging Initiative Adni Database - Human aging is a hot topic in biology, and it has been associated with DNA methylation changes at specific genomic sites. We aimed to study the changes of DNA methylation at a single-CpG-site resolution using peripheral blood samples from centenarians. - Source: PubMed
Publication date: 2018/02/02
Zeng QianChen XiaopingNing ChaoxueZhu QiaoYao YaoZhao YaliLuan Fuxin - To investigate the molecular mechanism associated with the signaling pathway of platinum drug administration, we focused on the C2H2-type zinc finger (ZNF) transcription factor gene family. Here we show cloning of a Krüppel-type ZNF gene, HKR1, which contains Krüppel-associated box (KRAB) domain and ZNF motifs. We found that mRNA expression of the HKR1 gene was induced in lung-cancer cell lines by exposure to cisplatin using Northern blot analysis. Moreover, we also found that HKR1 mRNA expression levels in lung cancers were higher than those in normal lung tissues, and that high expression levels in lung cancers were associated with antemortem platinum drug administration. These results suggest that HKR1 may be associated with the regulation of a signaling pathway involved in the progression of lung cancer or the acquisition of resistance to platinum drugs. - Source: PubMed
Oguri TKatoh OTakahashi TIsobe TKuramoto KHirata SYamakido MWatanabe H - A gene whose overexpression can endow Saccharomyces cerevisiae cells with resistance to HM-1 killer toxin was cloned from an S. cerevisiae genomic library. This gene, designated HKR1 (Hansenula mrakii killer toxin-resistant gene 1), contains a 5.4-kb open reading frame. The predicted amino acid sequence of the protein specified by HKR1 indicates that the protein consists of 1,802 amino acids and is very rich in serine and threonine, which could serve as O-glycosylation sites. The protein also contains two hydrophobic domains at the N-terminal end and in the C-terminal half, which could function as a signal peptide and transmembrane domain, respectively. Hkr1p is found to contain an EF hand motif of the calcium-binding consensus sequence in the C-terminal cytoplasmic domain. Thus, Hkr1p is expected to be a calcium-binding, glycosylated type I membrane protein. Southern and Northern (RNA) analyses demonstrated that there is a single copy of the HKR1 gene in the S. cerevisiae genome, and the transcriptional level of HKR1 is extremely low. Gene disruption followed by tetrad analysis showed that HKR1 is an essential gene. Overexpression of the truncated HKR1 encoding the C-terminal half of Hkr1p made the cells more resistant to HM-1 killer toxin than the full-length HKR1 did, demonstrating that the C-terminal half of Hkr1p is essential for overcoming the effect of HM-1 killer toxin. Furthermore, overexpression of HKR1 increased the beta-glucan content in the cell wall without affecting in vitro beta-glucan synthase activity, suggesting that HKR1 regulates beta-glucan synthesis in vivo. - Source: PubMed
Kasahara SYamada HMio TShiratori YMiyamoto CYabe TNakajima TIchishima EFuruichi Y