Ask about this productRelated genes to: BECN1 antibody
- Gene:
- BECN1 NIH gene
- Name:
- beclin 1
- Previous symbol:
- -
- Synonyms:
- ATG6, VPS30
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-27
- Date modifiied:
- 2016-10-05
- Gene:
- BECN2 NIH gene
- Name:
- beclin 2
- Previous symbol:
- BECN1P1
- Synonyms:
- -
- Chromosome:
- 1q43
- Locus Type:
- gene with protein product
- Date approved:
- 2010-06-29
- Date modifiied:
- 2015-05-06
Related products to: BECN1 antibody
Related articles to: BECN1 antibody
- Macroautophagy (hereafter referred to as autophagy) requires the coordinated action of approximately 20 (autophagy related) genes. Duplication of genes has had a major impact on the evolution of the autophagy pathway among major lineages. One duplication hotspot is in vertebrates. However, the exact duplication timing, post-duplication evolutionary divergence patterns, and its relation to functional differences among paralogs have not been investigated in detail. Here, we demonstrate that most genes were likely duplicated by whole-genome duplication events near the root of vertebrates. We compared the sequence and gene expression divergence between paralogs and categorized the evolutionary fates (i.e., how ancestral function is divided between paralogs). Within the paralog pairs that evolved most asymmetrically, namely , ( and ), and , one paralog likely retained the ancestral function, allowing the other to evolve under less constraint. While no obvious asymmetry was observed between and in non-mammalian vertebrates, experienced marked sequence divergence and expression level reduction in mammals, suggesting a shift in balance. Expression patterns among the ( and ), ( and ), and ( and ) pairs were more consistent with hypofunctionalization/dosage sharing, such that ancestral function depends on both paralogs. We also demonstrate that both and can support autophagy, whereas only , but not , has autophagic function and discuss the relationship between autophagic function and evolutionary divergence. The present detailed analysis of gene duplication in vertebrates provides a critical timeline for interpreting functional differentiation between homologs.: ATG: autophagy related; BLAST: Basic Local Alignment Search Tool; DKO: double knockout; GFP: green fluorescent protein; GLMM: generalized linear mixed model; KO: knockout; LC3: MAP1LC3; MEF: mouse embryonic fibroblast; ns: non-significant; PAML: Phylogenetic Analysis by Maximum Likelihood; RPKM: reads per kilobase per million mapped reads; SVA: surrogate variable analysis; TMM: trimmed mean of M values; TMR: tetramethylrhodamine; WT: wild type. - Source: PubMed
Publication date: 2026/01/24
Zhang SidiKoyama-Honda IkukoHiratsuka DaikiMizushima Noboru - Nutritional and cooling strategies to abate the negative effects of heat stress during the dry period have been used to improve the performance of dairy cattle. The objective of this study was to evaluate the effects of feeding an immunomodulatory supplement (OmniGen-AF, OMN) before, during, and after exposure to either heat stress or active cooling during the dry period on immune function and mammary development in dairy cows. During late lactation (at least 60 d before dry off), cows were provided with evaporative cooling systems (shade, fans, and soakers) and assigned to two groups: placebo (56 g/d of AB20 top-dressed; CON) or OmniGen-AF (OMN, 56 g/d top-dressed). Cows were dried off ~46 d before the expected calving date and further split into evaporative cooling (shade, fans, and soakers; CL) or heat stress (only shade; HT) pens. Thus, after dry off, there were four treatment groups: heat stress with placebo (HT, n = 17), HT with OMN supplementation (HT + OMN, n = 19), CL with placebo (CL, n = 16), and CL with OMN supplementation (CL + OMN, n = 11). From a subset of cows (n = 6-8 per group), four blood samples were collected during the dry period (-43, -39, -32, and -21 d relative to calving) to evaluate neutrophil function and blood hematology. In addition, mammary biopsies (4-6 cows/treatment) were collected at -43, -39, -32, and -21 d relative to calving to evaluate mammary gland gene expression and histology, i.e., Tdt dUTP nick-end labeling (TUNEL) and Ki67. Genes related to autophagy, apoptosis, and cell proliferation were analyzed by qRT-PCR. Relative to CL, HT downregulated the expression of beclin-2 () but upregulated the expression of beclin-1 () on days -43 and -39 relative to calving, respectively. Also, relative to CL, HT upregulated the expression of and on day -39 relative to calving. These differences in gene expression were followed by HT cows having a lower total cell apoptosis rate during involution relative to CL cows. Further to these effects, HT leads to a lower alveoli number relative to CL cows. As in the CL treatment, OMN cows have a higher total cell apoptosis rate and alveoli number relative to CON cows. In addition, OMN cows have higher total cell proliferation relative to CON. Prolactin (PRL) and cortisol concentrations were evaluated during the dry period at days -45, -26, -3, and -1 relative to calving. Relative to CL, HT cows had higher PRL at day -45 but lower PRL on day -1 relative to calving, and a similar trend was observed for cortisol concentrations. In summary, HT impacts mammary gland gene expression, compromises mammary involution, reduces alveoli number, and alters hormone dynamics throughout the dry period. Following the same trends as the CL treatment, OMN increases mammary gland turnover by having a higher cell apoptosis and cell proliferation rate and lower connective tissue relative to CON cows. - Source: PubMed
Publication date: 2025/10/27
Fabris Thiago FLaporta JimenaCorra Fabiana NTorres Yazielis MKirk David JChapman James DDahl Geoffrey E - AMBRA1 autophagy and beclin 1 regulator 1; ATG14 autophagy related 14; ATG5 autophagy related 5; ATG7 autophagy related 7; BECN1 beclin 1; BECN2 beclin 2; CC coiled-coil; CQ chloroquine CNR1/CB1R cannabinoid receptor 1 DAPI 4',6-diamidino-2-phenylindole; dCCD delete CCD; DRD2/D2R dopamine receptor D2 GPRASP1/GASP1 G protein-coupled receptor associated sorting protein 1 GPCR G-protein coupled receptor; ITC isothermal titration calorimetry; IP immunoprecipitation; KD knockdown; KO knockout; MAP1LC3/LC3 microtubule associated protein 1 light chain 3; NRBF2 nuclear receptor binding factor 2; OPRD1/DOR opioid receptor delta 1 PIK3C3/VPS34 phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4/VPS15 phosphoinositide-3-kinase regulatory subunit 4; PtdIns3K class III phosphatidylinositol 3-kinase; PtdIns3P phosphatidylinositol-3-phosphate; RUBCN rubicon autophagy regulator; SQSTM1/p62 sequestosome 1; UVRAG UV radiation resistance associated; VPS vacuolar protein sorting; WT wild type. - Source: PubMed
Publication date: 2023/07/13
Qiu XianxiuLi NaYang QifanWu ShuaiLi XiaohuaPan XuehuaYamamoto SohZhang XiaozheZeng JinchengLiao JiahaoHe CongcongWang RenxiaoZhao Yanxiang - Thymic stromal cells (TSCs) are critical regulators of T cell tolerance, but their basic biology has remained under-characterized because they are relatively rare and difficult to isolate. Recent work has revealed that constitutive autophagy in TSCs is required for self-antigen presentation and central T cell tolerance induction; however, the mechanisms regulating constitutive autophagy in TSCs are not well understood. Hydrogen peroxide has been shown to increase autophagy flux in other tissues, and we previously identified conspicuously low expression of the hydrogen peroxide-quenching enzyme catalase in TSCs. We investigated whether the redox status of TSCs established by low catalase expression regulates their basal autophagy levels and their capacity to impose central T cell tolerance. Transgenic overexpression of catalase diminished autophagy in TSCs and impaired thymocyte clonal deletion, concomitant with increased frequencies of spontaneous lymphocytic infiltrates in lung and liver and of serum antinuclear antigen reactivity. Effects on clonal deletion and autoimmune indicators were diminished in catalase transgenic mice when autophagy was rescued by expression of the Becn1 knock-in allele. These results suggest a metabolic mechanism by which the redox status of TSCs may regulate central T cell tolerance. - Source: PubMed
Publication date: 2022/09/26
Semwal Manpreet KHester Allison KXiao YangmingUdeaja ChiomaCepeda SergioVerschelde John SJones NicholasWedemeyer Sarah AEmtage SimonWimberly KymberlyGriffith Ann V - Macroautophagy/autophagy-related proteins regulate infectious and inflammatory diseases in autophagy-dependent or -independent manner. However, the role of a newly identified mammalian-specific autophagy protein-BECN2 (beclin 2) in innate immune regulation is largely unknown. Here we showed that loss of BECN2 enhanced the activities of NLRP3, AIM2, NLRP1, and NLRC4 inflammasomes upon ligand stimulations. Mechanistically, BECN2 interacted with inflammasome sensors and mediated their degradation through a ULK1- and ATG9A-dependent, but BECN1-WIPI2-ATG16L1-LC3-independent, non-canonical autophagic pathway. BECN2 recruited inflammasome sensors on ATG9A vesicles to form a complex (BECN2-ATG9A-sensors) upon ULK1 activation. Three soluble NSF attachment protein receptor (SNARE) proteins (SEC22A, STX5, and STX6) were further shown to mediate the BECN2-ATG9A-dependent inflammasome sensor degradation. Loss of BECN2 promoted alum-induced peritonitis, which could be rescued by the ablation of CASP1 in -deficient mice. Hence, BECN2 negatively regulated inflammasome activation to control inflammation, serving as a potential therapeutic target for the treatment of infectious and inflammatory diseases.: AIM2: absent in melanoma 2; ATG: autophagy related; BECN1: beclin 1; BMDC: bone marrow-derived dendritic cells; BMDM: bone marrow-derived macrophages; CASP1: caspase 1; CQ: chloroquine; gMDSC: granulocytic myeloid-derived suppressor cells; IL: interleukin; LPS: lipopolysaccharide; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; mMDSC: monocytic myeloid-derived suppressor cells; NLRC4: NLR family CARD domain containing 4; NLRP1: NLR family pyrin domain containing 1; NLRP3: NLR family pyrin domain containing 3; PECs: peritoneal exudate cells; PYCARD/ASC: apoptosis-associated speck-like protein containing a caspase activation and recruitment domain; SNAREs: soluble NSF attachment protein receptors; STX5: syntaxin 5; STX6: syntaxin 6; ULK1: unc-51 like autophagy activating kinase 1; WIPI: WD repeat domain, phosphoinositide interacting. - Source: PubMed
Publication date: 2021/06/21
Deng GuangtongLi ChaoranChen LangXing ChangshengFu ChuntangQian ChenLiu XinWang Helen YZhu MotaoWang Rong-Fu