Ask about this productRelated genes to: FERMT2 antibody
- Gene:
- FERMT2 NIH gene
- Name:
- fermitin family member 2
- Previous symbol:
- PLEKHC1
- Synonyms:
- mig-2, KIND2, UNC112B
- Chromosome:
- 14q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-23
- Date modifiied:
- 2015-09-11
Related products to: FERMT2 antibody
Related articles to: FERMT2 antibody
- Although there are several proteomic studies testing brain responses to glucocorticoids, there were no attempts to integrate these data and compare them with responses at the level of mRNAs. Furthermore, the utility of available data is compromised by changes in nomenclature and usage of different types of identifiers. Therefore, the aim of this study was to identify the most consistent changes in protein expression in standardized mouse, rat, and human datasets and compare them with transcriptomic responses to glucocorticoids. The analysis showed that the two most frequently and consistently detected proteins were ATP synthase F1 subunit beta (Atp5f1b) and aldolase, fructose-bisphosphate C (Aldoc), while the most consistent proteomic and transcriptomic findings included Aldoc, Plin4, Aqp4, Endod1, Glul, Anln, Aldh1l1, Parp1, Trf, Fermt2, Tmem63a, and Trim2. The study also revealed limitations of available proteomic data indicating significant gaps in knowledge. Finally, the study provides an integrated dataset with updated protein nomenclature and a complete set of major identifiers to facilitate usage of proteomic data. - Source: PubMed
Juszczak Grzegorz R - YAP and TAZ are transcriptional regulators essential for mechanotransduction, development, and tissue homeostasis, whose dysregulation is implicated in multiple diseases, including cancer. To identify key regulators of YAP/TAZ signaling required for breast cancer cell fitness, we performed CRISPR/Cas9-based loss-of-function genetic screens both in vitro and in vivo. A custom sgRNA library targeting 216 candidate YAP/TAZ modulators was screened across three breast cancer cell lines. Among these, FERMT2, a component of the integrin signaling pathway, consistently emerged as a strong drop-out hit, highlighting its essential role in sustaining YAP/TAZ-dependent fitness. Bioinformatic analysis of large-scale cancer datasets further revealed genetic co-dependency between FERMT2, YAP, and TAZ, particularly in tumors with high YAP/TAZ expression. Functional validation through FERMT2 knockout and silencing demonstrated its requirement for proliferation, anchorage-independent growth, and tumorigenicity in triple-negative breast cancer cells. FERMT2 loss impaired YAP/TAZ nuclear accumulation, reduced the expression of YAP/TAZ target genes, and decreased phosphorylation at key tyrosine residues. Mechanistically, FERMT2 regulates YAP/TAZ independently of the canonical Hippo pathway through integrin-mediated activation of FAK. Consistent with this, glucocorticoid-driven FAK activation restored YAP/TAZ signaling in FERMT2-depleted cells. Partial epistasis analyses also indicate that FERMT2 modulates actin-dependent regulation of YAP/TAZ. Together, these findings identify FERMT2 as a pivotal upstream regulator of YAP/TAZ via FAK signaling, demonstrate that YAP/TAZ are principal effectors of integrin activity, and suggest that FERMT2 may represent a selective vulnerability in cancers with elevated YAP/TAZ signaling. - Source: PubMed
Publication date: 2026/03/06
Chiesa AriannaPoli VittoriaCroci OttavioBiagioni FrancescaFuentes PatricioMarenda MattiaDondi AmbraRodighiero SimonaFilipuzzi MarcoSberna SilviaMarzi MatteoNicassio FrancescoZuber JohannesCampaner Stefano - Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, with its heterogeneous molecular profiles complicating prognosis prediction. Multi-omics profiling of clinical CRC specimens is particularly valuable for uncovering prognostic variables; however, such integrated studies remain scarce. Here, we applied the Multi-Omics Factor Analysis v2 framework to multi-omics data (mutations, miRNA, RNA, proteomics, phospho-proteomics) from the CPTAC-2 cohort and constructed a comprehensive CRC model. This approach identified a survival-associated latent variable, which we term the CRC Prognostic Latent Factor (CPLF). The prognostic relevance of CPLF was then rigorously validated across three independent multi-omics cohorts, encompassing 579 patients with CRC. CPLF primarily reflects extracellular matrix deposition in the tumour microenvironment, with Tensin 1 (TNS1) and Fermitin family homologue 2 (FERMT2) as the highest-weighted features. Single-cell and spatial transcriptomic analyses, supplemented by immunohistochemistry, localized CPLF-associated gene expression predominantly to myofibroblasts. Functionally, knockdown of Tensin 1 or FERMT2 in fibroblasts attenuated tumour growth in vivo. Consistently, these top-weighted components of CPLF upregulated fibronectin 1 (FN1) expression in myofibroblasts, thereby activating integrin signaling in cancer cells and enhancing tumour progression. Altogether, our findings unveil CPLF as a data-inherent multi-omics prognostic factor and establish the CPLF/FN1/integrin axis as a key pathway mediating myofibroblast-cancer cell crosstalk in CRC progression. - Source: PubMed
Publication date: 2025/12/17
Chen TianweiYang YebinShi JingDong FanheXie LesiShan YuqiangWang Xiang - Intensive-care-unit-acquired-muscle-weakness is a debilitating complication of sepsis, characterized by loss of muscle mass and functionality. Immobilization is an important trigger, but the role of disturbed mechanical signaling is incompletely understood. In health, the integrin-receptor-complex with key components Kindlin2 (KIND2/Fermt2) and integrin-linked-kinase (ILK/Ilk1) converses mechanical forces into biochemical signals to regulate muscle mass. We hypothesize that this complex, through key elements KIND2 and ILK, plays a role in sepsis-induced-muscle-weakness. - Source: PubMed
Publication date: 2025/12/12
Pacolet AlexanderDerese IngePauwels LiesPerre Sarah VanderSmits MaximeVan den Haute ChrisDerde SarahKoppo KatrienGijsbers RikLangouche Lies - Alzheimer's disease (AD) is the most prominent form of dementia worldwide. It is characterized by tau lesions that spread throughout the brain in a spatio-temporal manner. This has led to the prion-like propagation hypothesis implicating a transfer of pathological tau seeds from cell to cell. Human brain-derived extracellular vesicles (BD-EVs) isolated from the brain-derived fluid of AD patients contain seeds that contribute to this tau pathology spreading. Knowing the rich diversity of EVs, isolation of functional EV sub-populations is required to unravel their implication in the pathophysiology of AD. - Source: PubMed
Publication date: 2025/12/05
Oosterlynck MarieLeroux ElodieNamasivayam BalasubramaniamBouillet ThomasCaillierez RaphaelleLoyens AnneMazur DanielePerbet RomainLefebvre ChristopheAboulouard SoulaimaneMaurage Claude-AlainAccart BertrandBuée LucColin Morvane