GTF2H1 siRNA_Lentivectors
- Known as:
- GTF2H1 siRNA_Lentivectors
- Catalog number:
- i009277d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GTF2H1 siRNA_Lentivectors
Related genes to: GTF2H1 siRNA_Lentivectors
- Gene:
- GTF2H1 NIH gene
- Name:
- general transcription factor IIH subunit 1
- Previous symbol:
- -
- Synonyms:
- BTF2, P62, TFIIH
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-16
- Date modifiied:
- 2016-10-05
Related products to: GTF2H1 siRNA_Lentivectors
Related articles to: GTF2H1 siRNA_Lentivectors
- To identify rare and common copy number variants (CNVs) associated with strabismus and amblyopia. - Source: PubMed
Lee Kyoung A ViolaWhitman Mary C - BACKGROUND: Calorie restriction (CR) is known to decrease not only spontaneous but also chemical- and radiation-induced carcinogenesis. However, the mechanism of anti-cancer effect by CR is extremely complex and not fully understood. In this study, we focused on changes in autophagy-related proteins (LC3 and p62) as factors related to changes in nutritional status and the suppression of carcinogenesis by CR. METHOD: B6C3F1 male mice were exposed to 0 Gy or 3.8 Gy X-rays at 1 week of age, and then both groups were fed either a standard diet (95 kcal/week) or a calorie-restricted diet with approximately 30% fewer calories (65 kcal/week) from 7 weeks of age. Mice were sacrificed at several time points, and their livers were collected and analyzed. RESULTS: CR suppressed the development of liver tumors in the irradiated group during the study period. The expression level of LC3 did not change significantly with or without CR and irradiation. On the other hand, the expression of p62 was significantly and temporarily increased in the irradiated CR group, in which radiation carcinogenesis was suppressed. Using immunofluorescence analysis, we found cells expressed p62 strongly throughout the cytoplasm in the CR group. In some of the p62-strong positive cells, the disappearance of the cell nucleus and a decrease in the nuclear DNA content were observed, and it was not co-localized with the cell proliferation marker, suggesting that cell death had occurred. CONCLUSIONS: Long-term CR, which inhibits radiation carcinogenesis, did not significantly affect autophagy activity in the liver as determined by LC3-II levels. On the other hand, increased expression of p62 was observed in the CR group in which the anti-cancer effect was confirmed. In particular, p62 strongly positive cells with smaller or no nuclei were detected exclusively in the CR group, suggesting a novel p62-mediated mechanism in the suppression of radiation-induced liver carcinogenesis by CR. - Source: PubMed
Publication date: 2025/08/28
Nakayama TakafumiSuzuki KeijiMitsutake Norisato - Deficiency in DNA-damage repair (DDR) genes, often due to disruptive coding variants, is linked to higher cancer risk. Our previous study has revealed the association between rare loss-of-function variants in DDR genes and the risk of lung cancer. However, it is still challenging to study the predisposing role of rare regulatory variants of these genes. - Source: PubMed
Publication date: 2024/12/03
An MingxingChen CongcongXiang JunLi YangQiu PinyuTang YiruLiu XinyueGu YayunQin NaHe YuanlinZhu MengJiang YueDai JunchengJin GuangfuMa HongxiaWang ChengHu ZhibinShen Hongbing - Augmenter of liver regeneration (ALR) is believed to protect against acute kidney injury (AKI). The objective of this study was to investigate the mechanisms of ALR in the transition from AKI to chronic kidney disease (CKD). - Source: PubMed
Publication date: 2024/11/27
Wang ChunxiaZeng XujiaYang PengfeiWang GangZhang ZhengLiao Xiaohui - The fusion of autophagosomes and lysosomes is essential for the prevention of nonalcoholic fatty liver disease (NAFLD). Here, we generate a hepatocyte-specific CHIP knockout (H-KO) mouse model that develops NAFLD more rapidly in response to a high-fat diet (HFD) or high-fat, high-fructose diet (HFHFD). The accumulation of P62 and LC3 in the livers of H-KO mice and CHIP-depleted cells indicates the inhibition of autophagosome-lysosome fusion. AAV8-mediated overexpression of CHIP in the murine liver slows the progression of NAFLD induced by HFD or HFHFD feeding. Mechanistically, CHIP induced K63- and K27-linked polyubiquitination at the lysine 198 residue of STX17, resulting in increased STX17-SNAP29-VAMP8 complex formation. The STX17 K198R mutant was not ubiquitinated by CHIP; it interfered with its interaction with VAMP8, rendering STX17 incapable of inhibiting steatosis development in mice. These results indicate that a signaling regulatory mechanism involving CHIP-mediated non-degradative ubiquitination of STX17 is necessary for autophagosome-lysosome fusion. - Source: PubMed
Publication date: 2024/10/02
Rho HyunjinKim SeungyeonKim Seung UpKim Jeong WonLee Sang HoonPark Sang HoonEscorcia Freddy EChung Joon-YongSong Jaewhan