GTF2H1 antibody - N-terminal region (P100811_T100)
- Known as:
- GTF2H1 (anti-) - N-terminal region (P100811_T100)
- Catalog number:
- p100811_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GTF2H1 antibody - N-terminal region (P100811_T100)
Related genes to: GTF2H1 antibody - N-terminal region (P100811_T100)
- 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 antibody - N-terminal region (P100811_T100)
Related articles to: GTF2H1 antibody - N-terminal region (P100811_T100)
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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
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