Gas1, recombinant protein, 50 ug.
- Known as:
- Gas1, Rec. protein, 50 ug.
- Catalog number:
- PR15082-50
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- Gas1 recombinant protein 50 .
Related genes to: Gas1, recombinant protein, 50 ug.
- Gene:
- GAS1 NIH gene
- Name:
- growth arrest specific 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-23
- Date modifiied:
- 2016-10-05
Related products to: Gas1, recombinant protein, 50 ug.
Related articles to: Gas1, recombinant protein, 50 ug.
- Methanogens are central to global carbon cycling and among the largest biological sources of methane, a potent greenhouse gas. At the heart of their energy metabolism lies the Hdr-Vhu-Fwd super-assembly, which couples H oxidation with CO reduction through flavin-based electron bifurcation. Here we present the cryogenic electron microscopy structure of the Hdr-Vhu-Fwd super-assembly from Methanococcus maripaludis, revealing an 8 MDa complex comprising 252 polypeptide chains and over 600 redox cofactors. Cryo-electron tomography further support that this super-assembly forms an intact structure within the cytoplasm of intact cells. This architecture comprises two hexameric HdrABC-Vhu rings linked by a tetrameric FwdF core, forming a continuous, circular electron chain. In this unique arrangement, 12 polyferredoxin subunits (VhuB) connect the Vhu-Hdr and Fwd complexes, thereby coupling electron bifurcation with CO reduction and directly linking the last and the first step of methanogenesis. Moreover, we identify a modular variant of the complex in which the [NiFe]-hydrogenase Vhu is substituted by tungsten-containing formate dehydrogenase (FdhAB), indicating flexible integration of electron-input modules facilitating metabolic adaptation under diverse environmental conditions. Analysis of the taxonomic distribution reveals that this architecture is specific to class I methanogens and is distinct from the smaller Hdr-Fmd complex of class II. Together, our study reveals that the the Hdr-Vhu-Fwd super-assembly has a modular and adaptable bioenergetic assembly, suggesting a lineage-specific architecture to adapt to diverse anaerobic niches. - Source: PubMed
Publication date: 2026/07/08
Paul SophiaPascoa Tomas CKlamke Max ABohn StefanAbendroth FrankDeobald DarjaVázquez OlallaStripp Sven TSchuller Jan M - This study aimed to initially characterize the effects of GANT61, a Hedgehog (Hh) signaling pathway inhibitor, on the biological behaviors of ALK-positive anaplastic large cell lymphoma (ALK + ALCL) cell lines and explore its underlying mechanisms. Cell proliferation was determined by CCK-8 assays. Cell cycle distribution and apoptotic rates were assessed by flow cytometry. Differential gene analysis and pathway enrichment studies were conducted using datasets from the GEO database with R packages. Protein expression levels of apoptosis-related markers (Bcl-2, Bax, caspase-3, cleaved caspase-3) and signaling molecules (Gli1, PIK3IP1, Akt, phosphorylated Akt) were quantitatively examined by western blotting. Corresponding mRNA levels were quantified by qRT-PCR. GANT61 treatment inhibited proliferation in a dose- and time-dependent manner, induced cell cycle arrest, and promoted apoptosis in ALK + ALCL cell lines. Notably, PIK3IP1 expression was markedly reduced compared with normal lymphocyte controls, while GAS1 expression showed significant upregulation in ALK + ALCL cell lines. Gene Set Enrichment Analysis (GSEA) demonstrated significant enrichment of the PI3K/Akt and Hh signaling pathways. Mechanistically, GANT61 upregulated PIK3IP1 while downregulating both Gli1 protein level and Akt phosphorylation. The Gli-targeting agent GANT61 may inhibit ALK + ALCL cell growth, trigger cell cycle arrest and induce apoptosis through Gli1 inhibition, potentially leading to PIK3IP1 upregulation and subsequent attenuation of PI3K/Akt pathway activity. These findings indicate that the Hh-PIK3IP1-Akt signaling axis may participate in ALK + ALCL tumorigenesis, showing that conventional target drugs can be employed for ALK + ALCL treatment. - Source: PubMed
Publication date: 2026/01/23
Chen HongyuanGao JingjingLi ChuntuanHan YanLiu ShengquanZhu Xiongpeng - The 77PD quinone (77PDQ), a member of PPDQs family, can be frequently detected in environment and bioavailable to organisms. In nematodes, toxicity of 77PDQ on longevity and healthspan and underlying mechanism were determined. Exposure to 0.1-10 μg/L 77PDQ reduced lifespan and inhibited healthspan indicated by change of locomotion behavior during the aging. 77PDQ was accumulated in mitochondrion, and caused mitochondrial dysfunction. Activities of mitochondrial complex I/II and expression of component genes for complex I/II were inhibited by 77PDQ, and RNAi of component genes of gas-1 and mev-1 strengthened 77PDQ toxicity on longevity and healthspan. Additionally, expressions of hsp-6/60, mitochondrial UPR (mt UPR) marker genes, were inhibited by 10 μg/L 77PDQ, suggesting induction of suppression in mt UPR. 77PDQ toxicity on longevity and healthspan was also exacerbated by hsp-6/60 RNAi. Pharmacological treatment with cuminaldehyde inhibited 77PDQ toxicity on longevity and healthspan and in causing suppression in mt UPR. This beneficial effect of cuminaldehyde could be disrupted by gas-1, mev-1, hsp-6, and hsp-60 RNAi, which further confirmed role of these mitochondrial signals in controlling 77PDQ toxicity. Therefore, risk of 77PDQ exposure in inhibiting longevity and healthspan was suggested, which was associated with dysregulation of mitochondrial signals. - Source: PubMed
Publication date: 2026/01/19
Shu ChengjieHu DayuCao ShengqiHou BeiweiGu ShunlinFu LeiZhang FenglunWang Dayong - Prostate cancer (PCa) is a prevalent malignancy with a rising incidence. Advanced PCa, often resistant to therapy, remains a major clinical challenge, underscoring the need to identify novel molecular drivers. Utilizing transcriptomic data from the TCGA and GEO databases, we identified as a key candidate through WGCNA, differential expression analysis, and LASSO regression. Its clinical relevance was assessed via Kaplan-Meier survival analysis. Then, we validated expression patterns using immunohistochemistry and Western blot in normal and malignant prostate cell lines. The functional effects of on proliferation, migration, and invasion and mechanisms of such were evaluated through in vitro gain- and loss-of-function assays (CCK-8, Ki67 staining, wound healing, Transwell, Western blot, etc.). was significantly downregulated in PCa, and this low expression strongly correlated with adverse clinicopathological features, including advanced T stage, higher Gleason scores, and worse survival. Bioinformatically, high expression was associated with an activated anti-tumor immune microenvironment, characterized by enhanced CD8+ T cell infiltration, reduced M2 macrophage abundance, and upregulation of the immune checkpoint . In vitro, overexpression effectively suppressed PCa cell proliferation, migration, and invasion, while its knockdown promoted these malignant phenotypes. Mechanistically, enhances the expression of the and its downstream related molecules , , and ; upregulates DNA damage-protective genes ( and ); and enhances the expression of cell cycle regulator . This study establishes as a suppressor in PCa, which impedes tumor progression by regulating key molecules involved in cellular inflammation, cell cycle arrest, and DNA damage response. - Source: PubMed
Publication date: 2026/01/03
Pang ZhongqiWang JiansheXu YidanJi BoRen MinghuaDing Beichen - Recurrent miscarriage (RM) remains a significant clinical challenge due to insufficient understanding of decidual microenvironment dysfunction and limited effective therapeutic options. Current treatments primarily focus on immunomodulation and hormonal therapy, which often fail to address the underlying decidual communication defects. This study investigates growth arrest-specific gene 1 (GAS1) as a potential therapeutic target for RM by elucidating its role in extracellular vesicle (EV)-mediated decidual communication and developing a novel RNA nanotechnology-based delivery system for targeted uterine treatment. - Source: PubMed
Publication date: 2025/12/20
Li Yuan-XingWei Si-QiZheng Peng-Sheng