Ask about this productRelated genes to: MOBKL1A antibody
- Gene:
- MOB1B NIH gene
- Name:
- MOB kinase activator 1B
- Previous symbol:
- MOBKL1A
- Synonyms:
- MOB4A
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-11
- Date modifiied:
- 2015-08-25
Related products to: MOBKL1A antibody
Related articles to: MOBKL1A antibody
- This study focused on the role of Saikosaponin A (SSA), a triterpenoid saponin derived from Bupleurum root, in regulating lipid metabolism and obesity. Sprague-Dawley rats were fed a high-fat diet, and 3T3-L1 preadipocytes were transformed into mature adipocytes. SSA was administered to both rats and mature adipocytes at different concentrations. Dual-luciferase reporter assays and RNA immunoprecipitation were conducted to explore the interaction between MOB1B and miR-26b-5p. The protein expression levels of key browning markers, including peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), cytochrome c (CytoC), and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), were quantified via Western blotting. Oil Red O staining was utilized to evaluate the effect of SSA on lipid deposition, while hematoxylin and eosin staining was employed to assess lipid droplet accumulation in epididymal white adipose tissue (eWAT). Immunohistochemistry was used to determine MOB1B in eWAT. As detected, SSA promoted the browning of eWAT and 3T3-L1 adipocytes by modulating the miR-26b-5p/MOB1B axis. The browning effect was demonstrated by a decrease in lipid droplet buildup and an increase in thermogenic and adipogenic markers such as PPARγ, C/EBPα, CytoC, and PGC1α. This study not only clarifies the novel mechanism of SSA induced eWAT browning through miR-26b-5p/MOB1B axis, but also provides experimental basis for the development of obesity therapeutic strategies based on natural components. - Source: PubMed
Publication date: 2026/02/04
Su XinTongXu ManHuanSu MiaoShangDong ShiNiXia JingXin SongJian - Alternative splicing (AS) is a tightly regulated process that gives rise to proteins with distinct or even opposing functions. But cancer-specific alternative splicing of circRNA formation is less likely to be identified. We identified circFLNB by a circRNA microarray and validated it by quantitative reverse transcription PCR. The role of circFLNB in CRC progression was assessed both in vitro and in vivo, and its downstream target genes were identified and validated in CRC cells by bioinformatics analysis and confirmed by luciferase reporter assays. The dysregulated alternative splicing events and splicing factors in chemotherapy-induced CRC tissues were identified using RNA-seq and rMATS analysis. The clinical implications of circFLNB were assessed in CRC tissue using the nomogram algorithm. We found that circFLNB was weakly expressed in colorectal cancer tissues and cells and its expression was increased by chemotherapy. Functionally, circFLNB repressed the proliferation and invasion of CRC cells in vitro, as well as inhibited the growth of CRC xenografts in mice in vivo. Mechanistically, circFLNB inhibited the proliferation of CRC in vivo and in vitro by targeting the miR-3127-3p/MOB1B/Hippo pathway. Furthermore, our investigation indicated that splicing factors QKI and CELF4 are essential and sufficient for the circFLNB biogenesis through chemotherapy-regulated alternative splicing. A patient prognosis model based on circFLNB expression levels can effectively predict the prognosis of CRC patients. Our research demonstrated that QKI- and CELF4- dependent alternative splicing induced by chemotherapy promotes circFLNB biogenesis, which inhibits CRC tumorigenesis via binding with miR-3127-3p to regulate the MOB1B/Hippo pathway. - Source: PubMed
Publication date: 2025/07/18
Han YingXu XinyuePeng YinghuiZhu JiangTang YijiaWu WantaoGao YanJiang ZhaohuiZhang XiangyangZhang PengFei JiangCai ChangjingShen HongZeng Shan - Castration-resistant prostate cancer (CRPC) is an aggressive disease exhibiting multiple epigenomic subtypes: androgen receptor-dependent CRPC-AR, and lineage plastic subtypes CRPC-SCL (stem cell-like), CRPC-WNT (Wnt-dependent), and CRPC-NE (neuroendocrine). By transcriptomic profiling of tissue, and whole-genome sequencing (WGS) of tissue and cell-free DNA (cfDNA) from 500 samples, we relate genomic variants with epigenomic state. We find lineage plasticity is associated with higher epigenomic and genomic heterogeneity. Samples with CRPC-SCL show higher chromosomal instability. We find DNA alterations, particularly chromosomal rearrangements, in the YAP/TAZ pathway associated with CRPC-SCL. For example, complex rearrangements on chromosome 4, which are supported by patient-matched 3D genome architecture data, decrease promoter interactions of , a YAP/TAZ pathway inhibitor, with its enhancers. Together, the genomic variants in the pathway can predict CRPC-SCL with 79% accuracy. We show the utility of cfDNA WGS for joint inference of epigenomic state and genomic variants, which can guide patient stratification for clinical decisions. - Source: PubMed
Publication date: 2025/07/02
Roskes Marjorie LMartinez-Fundichely AlexanderCohen SandraBalaban MetinWong Chen KhuanLi WeilingGonzalez Tonatiuh ATehim Anisha BXu HaoElNaggar ShahdMyers MatthewBareja RohanDorsaint PrincescaGorski KathrynAsad MuhammadAssaad Majd AlRobinson Brian DSigouros MichaelBarnett EthanManohar JyothiTagawa ScottNanus DavidMolina AnaNauseef Jones TSternberg Cora NMosquera Juan MiguelScher Howard ISboner AndreaRaphael Benjamin JChen YuKhurana Ekta - Activation of the intrinsic regenerative potential of adult mammalian hearts by promoting cardiomyocyte proliferation holds great potential in heart repair. CAND1 (Cullin-associated and neddylation-dissociated protein 1) functions as a critical regulator of cellular protein homeostasis by fine-tuning the ubiquitinated degradation of specific abnormally expressed protein substrates. Here, we identified that cardiac-specific transgenic overexpression of CAND1 reduced the infarct size, restored cardiac function, and promoted cardiomyocyte proliferation after myocardial infarction in juvenile (7-day-old) and adult (8-week-old) mice. Conversely, CAND1 deficiency blunted the regenerative capacity of neonatal hearts after apex resection. MS and functional verification demonstrated that CAND1 enhanced the assembly of Cullin1, FBXW11(F-box/WD repeat-containing protein 11), and Mob1b (Mps one binder kinase activator 1b) complexes, and thus promotes the degradation of Mob1b. The ubiquitination of Mob1b occurred at K108 and was linked by K48 of ubiquitin. Mob1b deletion partially rescued the loss of regenerative capacity in neonatal hearts induced by CAND1 deficiency and improved cardiac function in adult mice post-MI. Moreover, CAND1 promoted the proliferation of human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Our data demonstrate that CAND1 promotes cardiomyocyte proliferation via FBXW11-mediated K48-linked ubiquitination degradation of Mob1b, and improves heart regeneration after cardiac injury. The findings provide a novel strategy to promote cardiac regeneration and repair. Schematic diagram of the role of CAND1 in regulating ubiquitination and degradation of Mob1b and cardiomyocyte proliferation and heart regeneration. Under CAND1-High condition, CAND1 promotes the incorporation of Cullin1, FBXW11, and Mob1b complexes, and accelerates SCF-mediated K48-linked ubiquitination of Mob1b at the K108 site, which leads to the degradation of Mob1b and thus suppresses the Hippo signaling pathway and facilitates cardiomyocyte proliferation and heart regeneration post-MI. - Source: PubMed
Publication date: 2025/06/24
Li XingdaZhang LingminTian TaoPei YaoWang KaileWang ShuangNing XuanZhao PinhanQu YueyingGao HaiyuLi ChenhongLiu XueningYang JimingZhang YingziGao HongbinXuan LinaZhang YangLu YanjieCai BenzhiYang BaofengPan Zhenwei - The Hippo signaling pathway is an evolutionarily conserved, tumor suppressor, stem cell pathway. This is the very less explored pathway in Breast Cancer. It is a crucial regulator of several biological processes, such as organ size, differentiation, tissue homeostasis, cellular proliferation, and stemness. Interestingly, deregulation of this pathway leads to tumorigenesis. Hence, the present study aims to identify the role of the Hippo signaling pathway in Breast Cancer. - Source: PubMed
Publication date: 2025/02/10
Bhavnagari Hunayna MShah Franky D