GTF2H1 (Human) IP-WB Antibody Pair
- Known as:
- GTF2H1 (Human) IP-Western Blot Antibody Pair
- Catalog number:
- H00002965-PW1
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- GTF2H1 (Human) IP- Antibody Pair
Related genes to: GTF2H1 (Human) IP-WB Antibody Pair
- 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 (Human) IP-WB Antibody Pair
Related articles to: GTF2H1 (Human) IP-WB Antibody Pair
- To identify rare and common copy number variants (CNVs) associated with strabismus and amblyopia. - Source: PubMed
Lee Kyoung A ViolaWhitman Mary C - 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 - Schizophrenia (SCZ) symptoms can be classified as positive and negative ones, each of which has distinct traits and possibly differences in gene expression and regulation. The co-expression networks linked to PANSS (Positive and Negative Syndrome Scale) scores were identified by weighted gene co-expression network analysis (WGCNA) using the expression profiles of miRNA and mRNA in the peripheral blood of first-episode SCZ patients. The heterogeneity between positive and negative symptoms was demonstrated using gene functional enrichment, gene-medication interaction, and immune cell composition analysis. Then, target gene prediction and correlation analysis of miRNA and mRNA constructed a symptom-related miRNA-mRNA regulatory network, screened regulatory pairs, and predicted binding sites. A total of six mRNA co-expression modules, two miRNA co-expression modules, and ten hub genes were screened to be significantly associated with positive symptoms; five mRNA co-expression modules and eight hub genes were correlated with negative symptoms. Positive symptom-related modules were significantly enriched in axon guidance, actin skeleton regulation, and sphingolipid signaling pathway, while negative symptom-related modules were significantly enriched in adaptive immune response, leukocyte migration, dopaminergic synapses, etc. The development of positive symptoms may have been influenced by potential regulatory pairings such as miR-98-5p-EIF3J, miR-98-5p-SOCS4, let-7b-5p-CLUH, miR-454-3p-GTF2H1, and let-7b-5p-SNX17. Additionally, immune cells were substantially connected with several hub genes for symptoms. Positive and negative symptoms in SCZ individuals were heterogeneous to some extent. miRNAs such as let-7b-5p and miR-98-5p might contribute to the incidence of positive symptoms by targeting mRNAs, while the immune system's role in developing negative symptoms may be more nuanced. - Source: PubMed
Publication date: 2024/01/24
Jin MengdiXie MengtongDong LinXue FengyuLi WeizhenJiang LintongLi JunnanZhang MinSong HaidengLu QingxingYu Qiong