Breast cancer tissue array paired with metastatic tumors, 96 samples (1.5mm) with IHC data Species Human Anatomic System Breast
- Known as:
- Breast cancer tissue array paired metastatic tumors, 96 samples (1.5mm) Immunohistochemistry data Species Human Anatomic Breast
- Catalog number:
- BRM961
- Product Quantity:
- 1.5 mm
- Category:
- Peptides
- Supplier:
- Pantomics
- Gene target:
- Breast cancer tissue array paired with metastatic tumors 96 samples (1.5mm) IHC data Species Human Anatomic System
Related genes to: Breast cancer tissue array paired with metastatic tumors, 96 samples (1.5mm) with IHC data Species Human Anatomic System Breast
- Gene:
- RUBCN NIH gene
- Name:
- rubicon autophagy regulator
- Previous symbol:
- KIAA0226
- Synonyms:
- rubicon, rundataxin
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-21
- Date modifiied:
- 2019-04-23
Related products to: Breast cancer tissue array paired with metastatic tumors, 96 samples (1.5mm) with IHC data Species Human Anatomic System Breast
Related articles to: Breast cancer tissue array paired with metastatic tumors, 96 samples (1.5mm) with IHC data Species Human Anatomic System Breast
- Activation of PINK1 and Parkin in response to mitochondrial damage initiates a response that includes phosphorylation of RAB7A at Ser72. Rubicon is a RAB7A binding negative regulator of autophagy. The structure of the Rubicon:RAB7A complex suggests that phosphorylation of RAB7A at Ser72 would block Rubicon binding. Indeed, in vitro phosphorylation of RAB7A by TBK1 abrogates Rubicon:RAB7A binding. Pacer, a positive regulator of autophagy, has an RH domain with a basic triad predicted to bind an introduced phosphate. Consistent with this, Pacer-RH binds to phosho-RAB7A but not to unphosphorylated RAB7A. In cells, mitochondrial depolarization reduces Rubicon:RAB7A colocalization whilst recruiting Pacer to phospho-RAB7A-positive puncta. Pacer knockout reduces Parkin mitophagy with little effect on bulk autophagy or Parkin-independent mitophagy. Rescue of Parkin-dependent mitophagy requires the intact pRAB7A phosphate-binding basic triad of Pacer. Together these structural and functional data support a model in which the TBK1-dependent phosphorylation of RAB7A serves as a switch, promoting mitophagy by relieving Rubicon inhibition and favoring Pacer activation. - Source: PubMed
Publication date: 2024/05/10
Tudorica Dan ABasak BishalPuerta Cordova Alexia SKhuu GraceRose KevinLazarou MichaelHolzbaur Erika L FHurley James H - Parkinson's disease (PD) is the second most common neurodegenerative disease, and its prevalence is increasing. Currently, no effective therapies for PD exist. Marine-derived natural compounds are considered important resources for the discovery of new drugs due to their distinctive structures and diverse activities. In this study, tetrahydroauroglaucin (TAG), a polyketide isolated from a marine sponge, was found to have notable neuroprotective effects on MPTP/MPP-induced neurotoxicity. RNA sequencing analysis and metabolomics revealed that TAG significantly improved lipid metabolism disorder in PD models. Further investigation indicated that TAG markedly decreased the accumulation of lipid droplets (LDs), downregulated the expression of RUBCN, and promoted autophagic flux. Moreover, conditional knockdown of Rubcn notably attenuated PD-like symptoms and the accumulation of LDs, accompanied by blockade of the neuroprotective effect of TAG. Collectively, our results first indicated that TAG, a promising PD therapeutic candidate, could suppress the accumulation of LDs through the RUBCN-autophagy pathway, which highlighted a novel and effective strategy for PD treatment. - Source: PubMed
Publication date: 2024/03/27
Yang PeiLiu YangTong Zhi-WuHuang Qian-HuiXie Xia-HongMao Shi-YuDing Jian-HuaLu MingTan Ren-XiangHu Gang - The effective treatment of nitrate (NO) in water as a nitrogen source and electrocatalytic NO reduction to ammonia (NH) (NRA) have become preferred methods for NO-to-NH conversion. Achieving efficient NO-to-NH conversion requires the design and development of electrode materials with high activity and efficiency for the electrocatalytic NRA reaction. Herein, based on the special properties of dodecahydro-closo-dodecaborate anions, a BCN matrix, loaded with platinum-group nanoparticles (namely, Pd/BCN, Pt/BCN, and Ru/BCN), was prepared using a simple method for the electrocatalytic NRA reaction. Results showed that Pd/BCN exerts the best catalytic effect on the NRA reaction. The NH production rate reached 12.71 mg h mg at -1.0 V vs. RHE. Faraday efficiency reached 91.79 %, which can be attributed to the more uniform distribution of the nanoparticles. Furthermore, Pd/BCN exhibited high cycling stability and resistance to ionic interference. Moreover, the density functional theory calculations indicated that small and well-distributed Pd nanoclusters in the BCN matrix have a large active surface area and promote the catalytic process. This study provides a new strategy to design catalysts for green ammonia synthesis. - Source: PubMed
Publication date: 2024/03/06
Wang ZhengxiXia ShiyingDeng XuefanBaryshnikov GlibKuklin ArtemÅgren HansZhang Haibo - Parasite-specific CD4 Th1 cell responses are the predominant immune effector for controlling malaria infection; however, the underlying regulatory mechanisms remain largely unknown. This study demonstrated that ATG5 deficiency in myeloid cells can significantly inhibit the growth of rodent blood-stage malarial parasites by selectively enhancing parasite-specific CD4 Th1 cell responses. This effect was independent of ATG5-mediated canonical and non-canonical autophagy. Mechanistically, ATG5 deficiency suppressed FAS-mediated apoptosis of LY6G ITGAM/CD11b ADGRE1/F4/80 cells and subsequently increased CCL2/MCP-1 production in parasite-infected mice. LY6G ITGAM ADGRE1 cell-derived CCL2 selectively interacted with CCR2 on CD4 Th1 cells for their optimized responses through the JAK2-STAT4 pathway. The administration of recombinant CCL2 significantly promoted parasite-specific CD4 Th1 responses and suppressed malaria infection. Conclusively, our study highlights the previously unrecognized role of ATG5 in modulating myeloid cells apoptosis and sequentially affecting CCL2 production, which selectively promotes CD4 Th1 cell responses. Our findings provide new insights into the development of immune interventions and effective anti-malarial vaccines.: ATG5: autophagy related 5; CBA: cytometric bead array; CCL2/MCP-1: C-C motif chemokine ligand 2; IgG: immunoglobulin G; IL6: interleukin 6; IL10: interleukin 10; IL12: interleukin 12; MFI: mean fluorescence intensity; JAK2: Janus kinase 2; LAP: LC3-associated phagocytosis; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; pRBCs: parasitized red blood cells; RUBCN: RUN domain and cysteine-rich domain containing, Beclin 1-interacting protein; STAT4: signal transducer and activator of transcription 4; Th1: T helper 1 cell; Tfh: follicular helper cell; ULK1: unc-51 like kinase 1. - Source: PubMed
Publication date: 2024/02/23
Gao YuanliChen SuilinJiao ShimingFan YonglingLi XiuxiuTan NieFang JiaqinXu LumingHuang YiZhao JingGuo ShuaiLiu TaipingXu Wenyue - Shear stress induced by urinary flow stimulates macroautophagy (hereafter referred to as autophagy) in kidney proximal tubule epithelial cells. Autophagy and selective degradation of lipid droplets by lipophagy contribute to tubule homeostasis by the production of ATP and control of epithelial cell size. Autophagy/lipophagy is controlled by a signaling cascade emanating from the primary cilium, localized at the apical side of epithelial cells. Downstream of the primary cilium, AMPK controls mitochondrial biogenesis on the one hand and autophagy/lipophagy on the other hand, which together increase fatty acid production that fuels oxidative phosphorylation to increase energy production. Recently, we reported that the co-transcriptional factors YAP1 and WWTR1/TAZ act downstream of AMPK to control autophagy. In fact, YAP1 and the transcription factor TEAD control the expression of RUBCN/rubicon. Under shear stress, YAP1 is excluded from the nucleus in a SIRT1-dependent manner to favor autophagic flux by downregulating the expression of RUBCN. When simulating a pathological urinary flow in murine proximal tubule kidney epithelial cells, we observe the nuclear retention of YAP1 and, consequently, high expression of RUBCN and inhibition of autophagic flux. Importantly, these findings were confirmed in biopsies of patients suffering from diabetic nephropathy, a major cause of chronic kidney disease. - Source: PubMed
Publication date: 2024/02/25
Claude-Taupin AuroreTerzi FabiolaCodogno PatriceDupont Nicolas