EIF3S9 Blocking Peptide
- Known as:
- EIF3S9 Blocking Peptide
- Catalog number:
- 33r-10226
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- EIF3S9 Blocking Peptide
Related genes to: EIF3S9 Blocking Peptide
- Gene:
- EIF3B NIH gene
- Name:
- eukaryotic translation initiation factor 3 subunit B
- Previous symbol:
- EIF3S9
- Synonyms:
- PRT1, eIF3b
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-26
- Date modifiied:
- 2016-10-05
Related products to: EIF3S9 Blocking Peptide
Related articles to: EIF3S9 Blocking Peptide
- Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with poor prognosis and limited therapeutic options. A disintegrin and metalloproteinase 12 (ADAM12) is aberrantly expressed in multiple cancers and has been implicated in tumor progression. However, its biological role and underlying mechanism in HCC remain unclear. - Source: PubMed
Publication date: 2026/05/06
Wu ShengdongZhu YongfeiXia YanWu ShengjunLu Caide - Dysfunction of vascular endothelial cells is recognized as a critical driver in pulmonary vascular remodeling of pulmonary hypertension (PH). Although interleukin-6 (IL-6) has been firmly established as an indispensable factor leading to pulmonary vascular remodeling, its downstream molecular mechanisms remain incompletely elucidated. Here, we discover that ubiquitin-specific protease 2a (USP2a) is upregulated in lung tissues of PH patients and preclinical PH models, and in IL-6-stimulated endothelial cells. Both the endothelial cell-specific Usp2a genetic deletion and the pharmacological inhibition of USP2a with the inhibitor ML364 alleviate experimental PH manifestations. Mechanistically, USP2a attenuates the degradation of methyltransferase-like 16 (METTL16) by deubiquitination. Notably, METTL16 reciprocally enhances USP2a expression via interactions with eIF3a and eIF3b in a methyltransferase activity-independent manner, establishing a self-reinforcing USP2a-METTL16 regulatory loop. Subsequent investigations reveal that METTL16 enhances N6-methyladenosine (mA)-mediated IL-6 receptor (IL-6R) mRNA stabilization, thereby promoting the expression of IL-6R. This study demonstrates that endothelial USP2a-METTL16 loop potentiates IL-6 signaling via IL-6R and represents a promising therapeutic target for PH. - Source: PubMed
Publication date: 2026/04/25
Zhu HanqingYuan PingWu XiangyangHuang YuxiaZhang WentianSun XingxingXu JianhuaZhou TianranXu JunfangChen LiYang WenlanLiu JinmingLiu HaipengGao FenghouGuo Jian - Skeletal muscle is the largest organ by mass in the human body, and its functional capacity depends on the precise coordination of protein synthesis, mitochondrial bioenergetics, and regenerative potential. Eukaryotic translation initiation factor 3 (eIF3), a 13-subunit complex (~800 kDa) best known for its multifaceted roles in cancer, is now emerging as a key translational regulator in skeletal muscle physiology and disease. Here, we present a perspective that synthesizes recent advances into a unifying "dual-phase guardian" model. In the first phase, eIF3f acts at the level of translation initiation as a scaffold bridging mTORC1 and S6K1, integrating anabolic and catabolic signals, particularly the MAFbx/Atrogin-1 ubiquitin-proteasome axis, to govern net protein synthesis and muscle mass. In the second phase, eIF3e remains bound to 80S ribosomes during early translation elongation (codons 1-60) of approximately 2700 mRNAs encoding mitochondrial and membrane-associated proteins, facilitating co-translational quality control through chaperone recruitment (e.g., CCT/TRiC). Haploinsufficiency of eIF3e in mice produces mitochondrial hyperfusion, diminished respiratory complex I activity, sarcomeric degeneration, and progressive loss of grip strength, a phenotype recapitulating features of mitochondrial myopathy. Complementing these findings, eIF3b supports satellite cell-mediated muscle regeneration by resolving RNA G-quadruplex structures in the 5'-UTR of Anp32e mRNA, while eIF3a modulates fibrotic remodeling through TGF-β/Smad3 signaling. We situate these subunit-level findings within the broader landscape of translational regulators in muscle (eIF2α/ISR, eIF5A, eEF2) and critically evaluate the translational potential and therapeutic challenges, including the absence of human clinical data, tissue-selectivity concerns, and species-specific limitations, that must be addressed before these mechanistic insights can inform treatment of sarcopenia, disuse atrophy, and mitochondrial myopathy. - Source: PubMed
Xia JianingLiao KexinWang JiahuanLu MinghaoMu YonghaoLin Yingying - - Source: PubMed
Publication date: 2026/04/16
Li YingYang ChengruCui GuoliGui ShiliangJia LinlinChen YuNiu HonglinXin Hua - Psoriasis is a systemic inflammatory skin disease for which new topical treatments are needed. Psoriatic inflammation is associated with overexpression of eukaryotic translation initiation factors (eIFs), which regulate gene expression in processes such as proliferation, apoptosis, and differentiation. However, their role in psoriasis remains unclear. - Source: PubMed
Publication date: 2026/03/20
Golob-Schwarzl NicoleBordag NatalieShirsath NiteshMüller Christin-ThereseEl-Heliebi AminWolf Peter