SIRT4 antibody - middle region (ARP32451_P050)
- Known as:
- SIRT4 (anti-) - middle region (ARP32451_P050)
- Catalog number:
- arp32451_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SIRT4 antibody - middle region (ARP32451_P050)
Related genes to: SIRT4 antibody - middle region (ARP32451_P050)
- Gene:
- SIRT4 NIH gene
- Name:
- sirtuin 4
- Previous symbol:
- -
- Synonyms:
- SIR2L4
- Chromosome:
- 12q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-20
- Date modifiied:
- 2014-11-19
Related products to: SIRT4 antibody - middle region (ARP32451_P050)
Related articles to: SIRT4 antibody - middle region (ARP32451_P050)
- Keratin19 (KRT19) is the smallest type I KRT protein which is a member of the keratin family. KRT19 has been reported as a diagnostic marker in several cancers, such as lung, breast and pancreatic cancer. However, the diagnostic value and potential role of KRT19 in colorectal cancer (CRC) remain to be explored. Our study confirmed the KRT19 expression pattern in CRC through publicly database and in CRC patient tissues with immunohistochemistry (IHC) and Western blot. Then, we carried out a series of malignant phenotype assays like colony formation assay, transwell migration and invasion experiments to definite the role of KRT19 on CRC cells proliferation, migration and invasion. Co-immunoprecipitation (co-IP) and Western blot were utilized to clarify the underlying molecular mechanisms of KRT19 in CRC. The data from GEPIA and CRC specimens displayed that KRT19 expression was increased and correlated with a poor clinical outcome. Our in vitro experiments confirmed that KRT19 promoted the proliferation, migration and invasion of CRC cells. Moreover, co-IP verified the interaction between KRT19 and SIRT4. KRT19 also activated the mTOR pathway which was illustrated by Western blot. Our research provides that KRT19 may be served as a diagnostic marker for CRC, and KRT19 promotes CRC progression through mTOR pathway by interacting with SIRT4. - Source: PubMed
Qiran ZhuYing CuiCheng ChengBomiao Zhang - Sirtuins represent a family of highly conserved enzymes, initially identified as Silent Information Regulator 2 (Sir2) in yeast, where they serve as fundamental determinants of longevity. Overexpression of Sir2 in yeast significantly extends lifespan, while its deletion leads to shortened longevity. In mammals, sirtuins (SIRT1-7) represent a conserved family of NAD-dependent deacylases with diverse catalytic activities. While most members primarily function as deacetylases, SIRT4 exhibits mono-ADP-ribosylation activity, and SIRT5 uniquely targets negatively charged acyl groups, including lysine succinylation, malonylation, and glutarylation. These enzymes act as critical intracellular sensors and regulators widely distributed across diverse tissues. By targeting a broad array of protein substrates, they regulate core biological processes-including genomic stability, metabolism, inflammation, and stress responses. As cardiovascular diseases (CVDs) remain the primary cause of global mortality, driven by complex pathologies such as chronic inflammation and metabolic dysregulation, the sirtuin network has emerged as an indispensable regulator of cardiovascular health. This review systematically elucidates the pivotal roles of sirtuins in cardiovascular homeostasis. We provide an in-depth, subcellular perspective on how nuclear, cytoplasmic, and mitochondrial sirtuins synergistically protect against cardiovascular remodeling, atherosclerosis (AS), and heart failure (HF). Particular emphasis is placed on the molecular mechanisms modulating macrophage polarization and the mitigation of vascular inflammation via the NF-κB signaling pathway. Furthermore, we assess the therapeutic promise of caloric restriction (CR) and pharmacological activators, incorporating recent human clinical evidence. We propose a framework matching sirtuin-based interventions to disease tempo, advocating isoform and compartment-specific strategies for acute and chronic CVDs. - Source: PubMed
Publication date: 2026/09/10
Gao MinLi LanlanLi LinWu HanyuWu YunkunFu Lei - Cellular pathways for experimental discovery provide a comprehensive overview of sirtuin biology and its critical involvement in HIV-associated neurocognitive disorders (HAND) and related neurodegenerative diseases, highlighting the translational potential of sirtuin-targeted therapeutic strategies. As NAD-dependent deacetylases and ADP-ribosyl transferases, sirtuins regulate diverse cellular processes, including stem cell maintenance, cellular proliferation, metabolic homeostasis, apoptosis, autophagy, oxidative stress responses, and genomic stability, all of which contribute to neuronal dysfunction and disease progression. This chapter focuses on key mammalian sirtuins, including SIRT1 and SIRT2, which are primarily localized within the nucleus and cytosol; mitochondrial sirtuins SIRT3, SIRT4, and SIRT5; and nuclear/nucleolar sirtuins SIRT6 and SIRT7. Here, a method with a detailed protocol to isolate compartment-specific sirtuin expression and activity was used: subcellular fractionation was performed using a subcellular fractionation kit to obtain cytosolic and nuclear fractions, while mitochondrial isolation was carried out using Tom20 antibody-conjugated magnetic microbeads. These approaches were applied to brain tissues from HIV-positive individuals, as well as to HIV-Tat-treated human microglial (HMC3) cells and astrocytes. This experimental framework enables accurate assessment of compartment-resolved sirtuin regulation in disease-relevant models. Collectively, the chapter highlights the protective roles of sirtuins in mitigating key pathogenic mechanisms underlying HAND and related neurodegenerative diseases. These findings support the emerging concept that sirtuins represent promising pharmacological targets for the development of novel therapeutic interventions in neurodegeneration and HIV-associated brain disorders. - Source: PubMed
Publication date: 2026/07/13
Chennakesavan KarthickSamikkannu Thangavel - Mitochondrial sirtuins integrate cellular metabolic and energetic state with post-translational regulation of mitochondrial proteins, thereby influencing bioenergetics, redox homeostasis, and metabolic flexibility. Despite extensive study of individual sirtuins, a comprehensive understanding of their function remains limited by methodological and conceptual challenges. These arise from the complex metabolic environment in which mitochondrial sirtuins act, including compartmentalized NAD pools, metabolite-driven non-enzymatic acylation, overlapping substrate specificities, and limited tools to accurately characterize enzyme-specific activity, particularly for SIRT4. This review aims to highlight current experimental approaches used to study mitochondrial sirtuins, and the need to integrate enzymatic measurements with metabolic and physiological readouts. We discuss the importance of considering mitochondrial spatial heterogeneity within cells, tissue-specific metabolic context, and temporal dynamics of metabolic state when interpreting sirtuin activity. Recent advances in quantitative proteomics, metabolite profiling, and mitochondria-specific analyses provide new opportunities to resolve these complexities. Moving forward, integrating these approaches with a systems-level and quantitative framework will be critical to fully understand how mitochondrial sirtuins orchestrate metabolic regulation across cellular and organismal scales. - Source: PubMed
Publication date: 2026/06/08
Kaur ArshdeepSeetharam Ullas Kolthur - Parkinson's disease (PD), the second most prevalent neurodegenerative disorder, is characterized by progressive loss of dopaminergic neurons in the substantia nigra. Although the molecular mechanisms of PD remain incompletely understood, mitochondrial dysfunction has emerged as a central pathological driver, highlighting the urgent need for therapies targeting mitochondrial homeostasis. In this study, we demonstrate that rhynchophylline (Rhy), a bioactive alkaloid from species, exerts neuroprotective effects by restoring mitochondrial dynamics. Thermal proteome profiling identified dihydrolipoamide acetyltransferase (DLAT) as a direct target of Rhy. Genetic ablation of DLAT induced mitochondrial fragmentation and abolished Rhy-mediated beneficial effects on mitochondrial structure and function. Mechanically, Rhy binds to the N-terminal lipoyl domain of DLAT, allosterically disrupting its interaction with sirtuin 4 (SIRT4) and subsequently enhancing DLAT lipoylation, a critical post-translational modification for mitochondrial energy metabolism. , Rhy administration ameliorated motor deficits and dopaminergic neurodegeneration in both the 6-OHDA-induced and A53T -synuclein transgenic PD mouse models. Single-nucleus RNA sequencing further highlighted the clinical relevance of DLAT dysregulation in PD. Collectively, our findings establish Rhy as a promising PD therapeutic candidate and delineate DLAT as a pivotal node in therapeutic targets by promoting mitochondrial fusion and bioenergetics, offering a novel mechanistic avenue for neuroprotection. - Source: PubMed
Publication date: 2026/06/11
Liang XiaominYang XunfangWang ShuhuiZhuo FangfangHou XingziTu PengfeiLiu YangZeng KewuZhang Qingying