Bioinformatics Analysis of data for comprehensive TILLING
- Known as:
- Bioinformatics Analysis data comprehensive TILLING
- Catalog number:
- XGC-BiRDS-TILLING-192
- Product Quantity:
- Dataset of 192 samples
- Category:
- -
- Supplier:
- Xcelris
- Gene target:
- Bioinformatics Analysis data for comprehensive TILLING
Related genes to: Bioinformatics Analysis of data for comprehensive TILLING
- 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: Bioinformatics Analysis of data for comprehensive TILLING
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Specifically designed for converting microscope slides and films/film slides into digital data formats with high resolution"(1-kit) Antibody microarray analysis kit(10-kit) Antibody microarray analysis kit(2-kit) Antibody microarray analysis kit(5-kit) Antibody microarray analysis kit1 X PBS with 0.05% Sodium Azide,, Western Blot Analysis1,1'-Dioctadecyl-3,3,3',3'-tetramethylindotricarbocyanine iodide, DiR, A lipophilic near-IR (NIR) fluorescent membrane probe used for labeling cells for long term analysis, 25mg10 X MOPS Buffer, Southern_Nothern Blot analysis10 x PCR buffer ,CHEMICALS AND CONSUMERABLES FOR PCR ANALYSIS,10X PBS with 0.5% Tween 20, pH 7.4., Western Blot Analysis10x Reactionbuffer for SB0081 ,CHEMICALS AND CONSUMERABLES FOR PCR ANALYSIS,10X TBS with Tween-20 V3, Western Blot Analysis10X TBS with Tween-20, Western Blot Analysis10X TBS with Tween-20, Western Blot Analysis10X TBS, Western Blot Analysis Related articles to: Bioinformatics Analysis of data for comprehensive TILLING
- Natural products are biologically active compounds used for therapeutic interventions for various diseases, particularly infections. Autophagy is an intracellular catabolic pathway involving lysosomal degradation and is closely associated with immunological pathways, effectively combating bacterial, viral, fungal, and parasitic infections. Accumulating evidence suggests that autophagy activation or inhibition by natural products promotes antimicrobial responses against various pathogens. Numerous natural products can modulate autophagy through diverse signaling pathways, suggesting their potential as a host-directed therapeutic strategy that may complement conventional drug regimens or help mitigate drug resistance in various infectious diseases. However, it remains largely unclear whether these effects are mediated by direct modulation of autophagy or indirectly through associated mechanisms, including enhanced immune defense, attenuation of pathological inflammation, or crosstalk with other organelle functions. Additionally, multiple pathogens can evade host responses; thus, autophagy activation may inadvertently create favorable conditions for certain pathogens. This review discusses the current knowledge of natural products in terms of their antimicrobial actions through autophagy regulation, particularly the roles of distinct natural product classes, such as polyphenols, alkaloids, terpenoids, quinones, peptides, and macrolides in modulating autophagy for potentially contributing to control various infectious diseases. Exploring the intricate molecular interplay between natural products and autophagy in limiting infections may provide valuable insights that could inform the development of innovative host-directed antimicrobial treatments based on autophagy regulation. 3-MA: 3-methyladenine; AM: alveolar macrophages; AMP: antimicrobial peptides; AMPK: 5' adenosine monophosphate-activated protein kinase; ARDS: acute respiratory distress syndrome; ART: artemisinin; ASFV: African swine fever virus; ATG: autophagy related; AZM: azithromycin; BafA1: bafilomycin A; BECN1: beclin 1; BMDM: bone marrow-derived macrophage; BNIP3: BCL2 interacting protein 3; BNIP3L: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CAMKK2: calcium/calmodulin-dependent protein kinase kinase 2; CBD: cannabidiol; CF: cystic fibrosis; CGA: chlorogenic acid; CGAS: cyclic GMP-AMP synthase; CHUK/IKKα: component of inhibitor of nuclear factor kappa B kinase complex; CLP: cecal ligation and puncture; CLR: clarithromycin; CMA: chaperone-mediated autophagy; CoV: coronavirus; DHT: dihydrotanshinone I; EGCG: epigallocatechin-3-gallate; EIF2A: eukaryotic translation initiation factor 2A; EIF2AK2: eukaryotic translation initiation factor 2 alpha kinase 2; ESKAPE: , and spp.; ESRRA: estrogen related receptor alpha; FOXO1: forkhead box O1; FUNDC1: FUN14 domain containing 1; HBV: hepatitis B virus; HCV: hepatitis C virus; HDT: host-directed therapy; HIV: human immunodeficiency virus; HMGB1: high mobility group box 1; HSV: herpes simplex virus; IAV: influenza A virus; ICT: isocryptotanshinone; IFN: interferon; IKBKB/IKKβ: inhibitor of nuclear factor kappa B kinase subunit beta; IL: interleukin; INH: isoniazid; IRF3: IFN regulatory factor 3; KEAP1: kelch like ECH associated protein 1; LAMP: lysosomal associated membrane protein; LAP: LC3-associated phagocytosis; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MDM: monocyte-derived macrophage; MDR: multidrug-resistant; MON: monotropein; Mtb: ; MTOR: mechanistic target of rapamycin kinase; mtROS: mitochondrial ROS; NET: neutrophil extracellular trap; NFE2L2/Nrf2: NFE2 like bZIP transcription factor 2; NFKB/NF-κB: nuclear factor kappa B; NLRP3: NLR family pyrin domain containing 3; NLRX1: NLR family member X1; NOTCH1: notch receptor 1; NTM: nontuberculous mycobacteria; OMS: ohmyungsamycin; PAK1: p21 (RAC1) activated kinase 1; PINK1: PTEN induced kinase 1; PKM/PKM2: pyruvate kinase M1/2; PLD: phospholipase D; PM: peritoneal macrophage; PPM1A: protein phosphatase, Mg2+/Mn2+ dependent 1A; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase and tensin homolog; RB1CC1/FIP200: RB1 inducible coiled-coil 1; RELA/p65: RELA proto-oncogene, NF-kB subunit; RIF: rifampicin; ROS: reactive oxygen species; RSV: resveratrol; RUBCN/rubicon: rubicon autophagy regulator; SAR: selective autophagy receptor; SIRT: sirtuin; STING1: stimulator of interferon response cGAMP interactor 1; STX17: syntaxin 17; Tat: trans-activator of transcription; TB: tuberculosis; TBK1: TANK binding kinase 1; TFEB: transcription factor EB; TLR: toll like receptor; TNA: tanshinone IIA; TNF: tumor necrosis factor; UA: ursolic acid; ULK1/Atg1: unc-51 like autophagy activating kinase 1; UPR: unfolded protein response; UVRAG: UV radiation resistance associated; VAMP8: vesicle associated membrane protein 8; VDR: vitamin D receptor; WIPI2: WD repeat domain, phosphoinositide interacting 2; ZFYVE1/DFCP1: zinc finger FYVE-type containing 1; ZIKV: Zika virus. - Source: PubMed
Publication date: 2026/04/28
Paik SeungwhaUm SoohyunKim In SooPark Eun-JinKim Kyung TaeBasu JoyotiOh Dong-ChanJo Eun-Kyeong - Traumatic brain injury (TBI) elicits robust neuroinflammation and oxidative stress, coupled with an acute inhibition of macro-autophagy (autophagy) in neurons and microglia. Rubicon (), a Beclin1 interacting protein that suppresses autophagy and mediates LC3-associated phagocytosis and endocytosis (LAP/LANDO), influences inflammatory signaling in metabolic, neurodegenerative, and inflammaging diseases; yet its role in acquired brain injury has not been defined. Using a controlled cortical impact model, we investigated the role of Rubicon in acute neuroinflammatory responses following injury by comparing wild-type and -mutant mice. Bulk-RNA sequencing of injured cortex revealed attenuated induction of inflammatory pathways and reduced activation of pro-inflammatory microglial/macrophage phenotype in injured -mutant mice. -mutant mice demonstrated less pronounced inhibition of autophagy during the acute phase of injury. Although the inflammatory differences were transient, Rubicon mutant mice exhibited improved motor coordination and gait stability during recovery. Proteomic analyses revealed the presence of a truncated Rubicon protein in the mutant mice and identified the negative regulator of reactive oxygen species (NRROS) as a novel interactor of Rubicon. Consistent with this interaction, -mutant mice displayed markedly reduced oxidative damage, indicated by decreased lipid peroxidation after injury. Together, these findings indicate that Rubicon promotes acute neuroinflammatory and oxidative stress responses following TBI by modulating autophagy and ROS production. Rubicon mediated pathways may serve as therapeutic targets that offer a neuroprotective strategy to improve outcomes after TBI. - Source: PubMed
Publication date: 2026/03/06
Thapa SagarinaMehrabani-Tabari AmirPettyjohn-Robin OliviaNguyen Dexter PhWeldemariam Mehari MSarkar ChinmoyKhan MaryamKane Maureen ALipinski Marta M - CD8+ T cells are capable of specifically targeting and eliminating malignant tumor cells, but tumor cells can develop resistance mechanisms to escape CD8+ T cell-mediated killing. Here, we performed a whole genome CRISPR-Cas9 knockout screen under CD8+ T cells pressure and identified the E3 ubiquitin ligase CUL5 as an essential factor required for escaping CD8+ T cells killing in bladder cancer cells. We found that CUL5 knockout promoted the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing both in vivo and in vitro. Mechanistically, CUL5 loss reduced the ubiquitination of PTBP1, which regulated alternative splicing of RUBCN pre-mRNA and led to an increase in the levels of the RUBCN-S isoform, thereby preventing immune evasion of bladder cancer cells by inhibiting autophagy. Importantly, CUL5 knockout significantly enhanced the efficacy of anti-PD-1 immunotherapy in a xenograft model. Collectively, these findings reveal a novel mechanism of bladder cancer immune evasion, providing potential targets for cancer immunotherapy. - Source: PubMed
Publication date: 2026/02/09
Gao XinchengYu YanchaoSun JiayinZhao HuayuanYou YongqiangShi XinWang KangHong SijiaXiong XingHuang ChaoZhang HuiJiang Guosong - Analysis of autophagy-related gene expression data identified RUBCN as a novel biomarker influencing the pathogenesis and progression of breast cancer, underscoring its potential as a therapeutic target. We analyzed multiple breast cancer sample datasets using bioinformatics tools and databases. A consensus prognostic model was constructed and validated across several independent datasets to further examine its association with patient outcomes. A series of bioinformatics analyses focused on RUBCN were conducted, including expression profiling, independent prognostic evaluation, immune correlation analysis, and survival analysis. RUBCN expression was verified in breast cancer cell lines and clinical tissue specimens via Western blotting, quantitative real-time reverse transcription PCR, and immunohistochemistry. Functional assays, such as the Cell Counting Kit-8 assay, 5-ethynyl-2'-deoxyuridine incorporation assay, wound healing assay, and Transwell invasion assay, were employed to evaluate the effects of RUBCN knockdown on breast cancer cell proliferation and invasion. Autophagic activity, indicated by LC3 and P62 levels, was measured via Western blot in RUBCN-knockdown breast cancer cells with or without chloroquine treatment. Elevated expression of multiple autophagy-related genes was observed in breast cancer. The consensus prognostic model accurately predicted survival across multiple datasets, with RUBCN emerging as a key gene whose expression levels were significantly correlated with patient prognosis. Enrichment analysis indicated that RUBCN likely promotes breast cancer progression by regulating cell cycle and invasion processes. Further investigation revealed a negative correlation between RUBCN expression levels and immune cell infiltration, suggesting a potential role in mammary tumorigenesis through mediating immune evasion by suppressing immune cell infiltration. Immunohistochemical results confirmed upregulated RUBCN expression in carcinoma tissues. Knockdown of RUBCN was shown to suppress the proliferative and invasive abilities of breast cancer cells. Mechanistically, RUBCN knockdown impaired autophagic flux, as evidenced by altered LC3 and P62 levels upon chloroquine treatment. Together, these findings establish RUBCN as a promising therapeutic target in breast cancer. Future studies should emphasize in vivo functional validation using animal models and screen for targeted agents capable of modulating RUBCN expression or activity, thereby facilitating the development of innovative therapeutic strategies for breast cancer treatment. - Source: PubMed
Publication date: 2026/01/27
Yang Dong DongLiu Cheng HaoJia Sheng QiuXue Ze KuanZhang Ming MingYang RuiHuang Yong ZhouZhao Xin ChunHan Bao SanNie Sheng DongHuang Gui LinHou Ji Xue - Rubicon (RUN domain Beclin-1-interacting and cysteine-rich-containing protein) is a negative regulator of autophagy in nucleated cells; however, its role in platelets is unstudied. Here, we identify an autophagy-independent role for Rubicon in arterial thrombosis. Mice with a platelet/megakaryocyte-specific deletion of Rubicon (RUBCN-/-) showed normal circulating platelet counts, with a slight increase in platelet size. The basal levels of autophagy-related, vesicle-elongation proteins (ie, ATG5, ATG7, syntaxin 17, LC3, and Rab7) were unaffected, and there was no disruption in canonical platelet signaling pathways upon activation. Platelet secretion from all 3 granule classes remained intact. Aggregation/Agglutination in response to thrombin, convulxin, or botrocetin was unaffected. There was no overt defect in activation-dependent autophagic flux (ie, loss of LC3 or p62). However, RUBCN-/- mice had a significant thrombosis defect in the FeCl3-induced, carotid artery injury model, but no defect in the tail-transection hemostasis model. An intrinsic platelet defect was confirmed using microfluidics, in which RUBCN-/- platelets had reduced collagen binding under flow at high shear flow but not low shear. RUBCN-/- platelets also showed impaired surface exposure of phosphatidylserine (PS) after thrombin and convulxin activation, though there was no effect on total anoctamin 6, which contributes to PS exposure. There was no effect on platelet endocytosis, and only modest reductions in mitochondrial membrane potential with a slight delay in clot contraction, suggesting that Rubicon contributes to late stages of platelet function. Collectively, our findings demonstrate that Rubicon contributes to thrombosis and procoagulant platelet formation in a manner that appears independent of classical autophagy. - Source: PubMed
Alfar Hammodah RDriehaus Elizabeth RSmith Alexis NCoenen Daniëlle MMahmood Dlovan F DWood Jeremy PWhiteheart Sidney W