更新于：2024-09-19

BAZ

更新于：2024-09-19

基本信息

别名

ASIP、Atypical PKC isotype-specific-interacting protein、Baz

+ [12]

简介

Adapter protein involved in asymmetrical cell division and cell polarization processes (PubMed:27925688, PubMed:10954424). Seems to play a central role in the formation of epithelial tight junctions (PubMed:27925688). Targets the phosphatase PTEN to cell junctions (By similarity). Involved in Schwann cell peripheral myelination (By similarity). Association with PARD6B may prevent the interaction of PARD3 with F11R/JAM1, thereby preventing tight junction assembly (By similarity). The PARD6-PARD3 complex links GTP-bound Rho small GTPases to atypical protein kinase C proteins (PubMed:10934474). Required for establishment of neuronal polarity and normal axon formation in cultured hippocampal neurons (PubMed:19812038, PubMed:27925688).

关联

100 项与 BAZ 相关的临床结果

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100 项与 BAZ 相关的转化医学

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0 项与 BAZ 相关的专利（医药）

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337

项与 BAZ 相关的文献（医药）

2024-11-01·The Journal of Nutritional Biochemistry

The protective effect of dulcitol on lipopolysaccharide-induced intestinal injury in piglets: mechanistic insights

Article

作者: Liang, Shiyue ; Mu, Shuqin ; Wang, Han ; Zhong, Ruqing ; Li, Ning ; Zheng, Zi ; Chen, Liang ; Han, Hui ; Yan, Jun ; Liu, Zhengqun

This study investigated the protective effect of dulcitol on LPS-induced intestinal injury in piglets and explored the underlying molecular mechanisms. A total of 108 piglets were divided into three groups: CON, LPS, and DUL. The CON and LPS groups were fed a basal diet, the DUL group was fed a diet supplementation with 500 mg/kg dulcitol. On day 29, 6 piglets in the LPS and DUL groups were injected with 100 μg/kg BW of LPS. At 4 h post-challenge, all pigs were slaughtered, and colonic samples were collected. Results showed that dulcitol supplementation boosted intestinal barrier function in LPS-challenged piglets by enhancing intestinal morphology and integrity, and increasing the gene expression of zonula occludens-1, claudin-1, and occludin in the colonic mucosa (P <0.05). Metabolomics showed DUL supplementation mainly increased (P <0.05) the metabolites related to steroid and vitamin metabolism (Cholesterol and Vitamin C). Proteomics showed that dulcitol supplementation altered the protein expression involved in maintaining barrier integrity (FN1, CADM1, and PARD3), inhibiting inflammatory response (SLP1, SFN, and IRF3), and apoptosis (including FAS, ING1, BTK, MTHFR, NOX, and P53BP2) in LPS-challenged piglets (P <0.05). Additionally, dulcitol addition also suppressed the TLR4/NF-κB signaling pathway and apoptosis in mRNA and protein levels. Dulcitol increased the abundance of short-chain fatty acid-producing bacteria (Lactobacillus, Blautia, and Faecalibacterium) at the genus level, but decreased the relative abundance of Proteobacteria at the phylum level and Pseudomonas and Delftia at the genus level in piglets (P < 0.05). In conclusion, these results suggested that the addition of dulcitol alleviated LPS-induced intestinal barrier injury in piglets, probably by maintaining its integrity, inhibiting the TLR4/NF-κB signaling pathways and apoptosis, and modulating the gut microbiota. Therefore, dulcitol can be considered a potential dietary additive for improving intestinal health in pig models.

2024-10-01·Developmental Biology

Par3/bazooka binds NICD and promotes notch signaling during Drosophila development

Article

作者: Collu, Giovanna M ; Mlodzik, Marek ; Koca, Yildiz ; Vuong, Linh T ; Wu, Jun ; Bala Tannan, Neeta

The conserved bazooka (baz/par3) gene acts as a key regulator of asymmetrical cell divisions across the animal kingdom. Associated Par3/Baz-Par6-aPKC protein complexes are also well known for their role in the establishment of apical/basal cell polarity in epithelial cells. Here we define a novel, positive function of Baz/Par3 in the Notch pathway. Using Drosophila wing and eye development, we demonstrate that Baz is required for Notch signaling activity and optimal transcriptional activation of Notch target genes. Baz appears to act independently of aPKC in these contexts, as knockdown of aPKC does not cause Notch loss-of-function phenotypes. Using transgenic Notch constructs, our data positions Baz activity downstream of activating Notch cleavage steps and upstream of Su(H)/CSL transcription factor complex activity on Notch target genes. We demonstrate a biochemical interaction between NICD and Baz, suggesting that Baz is required for NICD activity before NICD binds to Su(H). Taken together, our data define a novel role of the polarity protein Baz/Par3, as a positive and direct regulator of Notch signaling through its interaction with NICD.

2024-08-01·Molecular Biology of the Cell

A novel protein Moat prevents ectopic epithelial folding by limiting Bazooka/Par3-dependent adherens junctions

Article

作者: Weng, Mo ; Joo, Minsang ; Fessahaye, Ferdos ; Nguyen, Jacqueline ; Gu, Lingkun ; Brar, Jasneet ; Lee, Joan ; Teng, Marissa ; Sauceda, Rolin

Contractile myosin and cell adhesion work together to induce tissue shape changes, but how they are patterned to achieve diverse morphogenetic outcomes remains unclear. Epithelial folding occurs via apical constriction, mediated by apical contractile myosin engaged with adherens junctions, as in Drosophila ventral furrow formation. While it has been shown that a multicellular gradient of myosin contractility determines folding shape, the impact of multicellular patterning of adherens junction levels on tissue folding is unknown. We identified a novel Drosophila gene moat essential for differential apical constriction and folding behaviors across the ventral epithelium which contains both folding ventral furrow and nonfolding ectodermal anterior midgut (ectoAMG). We show that Moat functions to downregulate polarity-dependent adherens junctions through inhibiting cortical clustering of Bazooka/Par3 proteins. Such downregulation of polarity-dependent junctions is critical for establishing a myosin-dependent pattern of adherens junctions, which in turn mediates differential apical constriction in the ventral epithelium. In moat mutants, abnormally high levels of polarity-dependent junctions promote ectopic apical constriction in cells with low-level contractile myosin, resulting in expansion of infolding from ventral furrow to ectoAMG, and flattening of ventral furrow constriction gradient. Our results demonstrate that tissue-scale distribution of adhesion levels patterns apical constriction and establishes morphogenetic boundaries.

项与 BAZ 相关的新闻（医药）

2024-02-08

·今日头条

抑制癌症发生！香港大学最新研究：揭示肝癌潜在预防靶点

本文为转化医学网原创，转载请注明出处作者：Rainbow 导读： Par-3家族细胞极性调节因子（PARD3）是一种细胞蛋白，对于不对称细胞分裂和极化生长至关重要。 2月6日，香港大学研究学者在期刊《Journal of Experimental & Clinical Cancer Research》上在线发表题为“PARD3 drives tumorigenesis through activating Sonic Hedgehog signalling in tumour-initiating cells in liver cancer”的研究论文，本研究揭示了PARD3作为潜在的肝癌预防靶点，通过调控TIC的功能发挥作用。 https://jeccr-biomedcentral-com.libproxy1.nus.edu.sg/articles/10.1186/s13046-024-02967-3 研究背景 01 原发性肝癌是全球第六大常见癌症和第三大致命癌症，2023年仅在美国就估计有41,210例新病例和29,380例死亡病例。肝细胞癌（HCC）是主要的原发性肝癌，通常在晚期被诊断，并且预后不佳。肝细胞癌（HCC）被认为是一种异质性疾病，肿瘤组织中包含具有不同基因表达特征和分子功能的癌细胞群。HCC的异质性由具有干细胞样特性的亚群细胞——肿瘤起始细胞（TICs）维持。TICs通过自我更新和分化能力导致肿瘤的异质结构，并且由于这些特性，导致HCC治疗失败和复发。早期肝细胞癌发生的分子机制尚待阐明。现有证据表明，TICs在肝癌发生中起着重要作用。具体而言，肝祖细胞作为癌变的细胞来源，在慢性肝病引起的分子事件中经历一系列变化，包括但不限于持续的DNA损伤和增加的染色体不稳定性。因此，肝祖细胞逐渐转化为TICs，进一步启动肿瘤发生和进展。维持TICs干细胞特性的信号通路和分子一直是癌症治疗研究的热门话题。 Par-3家族细胞极性调节蛋白（PARD3）是Par极性复合物的成员，它控制着细胞极性。PARD3在与空间不对称性相关的生物过程中起着重要作用，例如非对称细胞分裂（ACD），在TICs中尤其高度保守。通过ACD，TICs产生大量肿瘤细胞群体，同时保持具有干细胞特性的子细胞群体。已报道PARD3在多种恶性肿瘤的进展中发生异常调节并参与其中。最近的研究表明，在细胞转化过程中，细胞极性机制可能参与了致癌活动。然而，PARD3调节肝癌发生的具体机制尚不清楚。研究发现 02 本研究系统地研究了PARD3在肝癌发生中的作用。研究人员发现PARD3在自发性HCC小鼠模型的肿瘤发生阶段上调。PARD3在饮食诱导的肝癌发生中的重要作用已通过功能丧失和获得研究得到证实。PARD3过表达导致原位HCC模型中CD133+ TICs的富集。机制上，PARD3通过激活SHH信号传导来维持CD133+细胞的干性。研究证明PARD3是抑制肝癌发生的潜在靶点。研究结果 03 综上所述，本研究揭示了PARD3作为潜在的肝癌预防靶点，通过调控TIC的功能发挥作用。参考资料： https://jeccr-biomedcentral-com.libproxy1.nus.edu.sg/articles/10.1186/s13046-024-02967-3 注：本文旨在介绍医学研究进展，不能作为治疗方案参考。如需获得健康指导，请至正规医院就诊。热门·直播/活动 🕓 上海｜3月01日-02日 ▶第三届长三角单细胞组学技术应用论坛暨空间组学前沿论坛将在上海召开，诚邀您的参与！点击对应文字查看详情

临床研究