AMOTL2
- Known as:
- AMOTL2
- Catalog number:
- 001536A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AMOTL2
Related genes to: AMOTL2
- Gene:
- AMOTL2 NIH gene
- Name:
- angiomotin like 2
- Previous symbol:
- -
- Synonyms:
- LCCP
- Chromosome:
- 3q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-24
- Date modifiied:
- 2016-10-05
Related products to: AMOTL2
Related articles to: AMOTL2
- Angiomotin-like protein 2 (AMOTL2) regulates cell polarity and cytoskeletal regulation, but its role in gastric cancer (GC) remains undefined. Here, we show that AMOTL2 is frequently downregulated in GC tissues and cell lines, and its low expression is associated with deeper tumor invasion, lymph node metastasis, and shorter overall survival. Gain- and loss-of-function assays demonstrated that AMOTL2 suppresses GC cell proliferation, migration, and invasion. AMOTL2 overexpression also impaired endothelial and lymphatic-endothelial tube formation and reduced the expression of angiogenic and lymphangiogenic factors. In the subcutaneous, orthotopic, and popliteal lymph node metastasis models, AMOTL2 inhibited tumor growth and lymphatic dissemination. Mechanistically, AMOTL2 suppressed TGF-β/Smad signaling, as evidenced by reduced BMP2 and TGF-β1 expression, decreased Smad1/5/9 and Smad2/3 phosphorylation, and impaired Smads nuclear accumulation. Notably, pharmacological Smad1/5/9 activation by SB4 partially reversed the suppressive phenotypes of AMOTL2 and . Co-immunoprecipitation, GST pull-down, and ubiquitination assays identified SMURF1 as an AMOTL2-interacting E3 ubiquitin ligase that binds through its WW domains and promotes AMOTL2 ubiquitination and proteasomal degradation. AMOTL2 restoration counteracted SMURF1-driven malignant phenotypes. Collectively, these findings define AMOTL2 as a potential suppressor of GC progression that is destabilized by SMURF1, suggesting that the SMURF1-AMOTL2-Smad signaling axis may contribute to GC progression and lymphatic dissemination, representing a candidate therapeutic target that warrants further validation. - Source: PubMed
Publication date: 2026/08/11
Wang HuizhenYang BoLin ChangqingWang YigaoLu YidaLi JingLi JianhuiYu KexunWang MingliangLiu PengpengWang YuexiangLi Yongxiang - The Hippo pathway is a central regulator of tissue homeostasis, organ growth, and tumorigenesis. NF2 (Neurofibromin 2, also known as Merlin) functions as a pivotal upstream component that integrates biochemical and mechanical cues to restrain the activity of the transcriptional coactivators Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), thereby limiting cell proliferation. In addition, NF2 regulates members of the Motin family proteins (AMOT, AMOTL1, and AMOTL2) through ubiquitin-mediated turnover to modulate YAP/TAZ signaling output. Moreover, NF2 controls AMOT proteolytic processing to reorganize the actin cytoskeleton, thereby influencing cell motility. Through these mechanisms, NF2 establishes a multilayered regulatory system that coordinates cell proliferation and cell migration. This review summarizes recent advances in how NF2 regulates YAP/TAZ and AMOT functions, focusing on their roles in tumor formation, metastasis, and angiogenesis. - Source: PubMed
Publication date: 2026/08/31
Wang YuYu Fa-Xing - Inhibitor of nuclear factor kappa-B kinase subunit epsilon (IKBKE), a member of the serine/threonine kinase family, is an important oncogene in glioblastoma. IKBKE is involved in the progression of multiple tumours in glioblastoma (GBM), including tumour invasion, migration, and proliferation. Here, we report an IKBKE-angiomotin-like protein 2 (Amotl2)-yes-associated protein 1 (YAP1) axis in which IKBKE inhibits the protein expression of Amotl2, while Amotl2 regulates the nuclear transport of the YAP1 protein, which has been implicated in brain tumour development and progression. Data analysis of multiple IKBKE mRNA databases of glioma and immunohistochemical analysis of a tissue chip indicated that higher IKBKE expression was associated with higher malignancy and shorter survival in glioma patients. IKBKE downregulation significantly inhibited GBM cell proliferation and restrained tumour growth in a GBM mouse model. Moreover, IKBKE phosphorylates Amotl2, promoting Amotl2 ubiquitination and degradation, leading to YAP1 entry into the nucleus and the activation of downstream genes. In summary, our results are the first to show that IKBKE phosphorylates Amotl2 and that GBM cell proliferation is regulated by the IKBKE↑-Amotl2↓-YAP1↑ axis. - Source: PubMed
Publication date: 2026/07/24
Guo GaochaoSun YanHong RujunLu YalinChen XingjieZhao LimingLi ChaoyueLiu YangHuang Qiang - Knowledge of the role of IgA isotype autoantibodies in systemic lupus erythematosus (SLE) is lacking. We aimed to explore associations between serum IgA autoantibody profiles and SLE clinical phenotypes using an unbiased approach. - Source: PubMed
Publication date: 2026/07/15
Eades Laura EPapadaki ArtemisLennard KatieHoi Alberta YKandane-Rathnayake RangiMorand Eric FFiggett William AVincent Fabien B - Celastrol is a promising therapeutic candidate for cancers, metabolic diseases, and autoimmune disorders. However, recent studies demonstrated consecutive administration of celastrol at anticancer doses may induce severe heart injuries, which significantly limited its clinical translation. This study aimed to investigate the cellular target and potential mechanism underlying celastrol-induced cardiotoxicity. Consecutive i.p. injection of celastrol for 14 days induces cardiotoxicity in mice, as evidenced by reduced heart-to-body weight ratio, decreased cardiac output and stroke volume, and increased serum cardiac enzymes and proinflammatory cytokine levels in heart tissues. At the cellular level, celastrol triggered mitochondrial dysfunction and promoted cardiomyocyte apoptosis through activation of the mitochondrial pathway, as evidenced by altered B-Cell Lymphoma 2/Bcl-2-Associated X Protein (Bax/Bcl-2) ratio and expression of Cysteinyl aspartate specific proteinase 3 (caspase-3). Mechanistically, we identified Angiomotin-Like Protein 2 (AMOTL2) as a direct cellular target of celastrol using activity-based protein profiling (ABPP). Celastrol-AMOTL2 binding initiated a signaling cascade through Hippo pathway activation, promoting Yes-Associated Protein 1 (YAP1) phosphorylation and subsequent degradation. Knockdown of AMOTL2 by short hairpin RNA attenuated celastrol-induced cardiomyocyte apoptosis by enhancing YAP1 expression and mitochondrial biogenesis. These findings demonstrate that celastrol induces cardiotoxicity by directly targeting AMOTL2 and disrupting YAP1/PGC-1α/TFAM-dependent mitochondrial biogenesis. - Source: PubMed
Publication date: 2025/12/16
Shang HuiyingCheng HongboZhou WeiTang XianglinHan WeiyeZhang XiaotongXiao ChengrongGao YehuiLiu XianGao Yue