Ask about this productRelated genes to: MLF2 Blocking Peptide
- Gene:
- MLF2 NIH gene
- Name:
- myeloid leukemia factor 2
- Previous symbol:
- -
- Synonyms:
- NTN4
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-02
- Date modifiied:
- 2019-01-14
Related products to: MLF2 Blocking Peptide
Related articles to: MLF2 Blocking Peptide
- The use of hyaluronic acid (HA) fillers is rising globally. Traditionally, the rheology of HA fillers has been subject to investigations for their use in facial soft tissues. Hitherto, there has been a significant gap in understanding their rheologic properties in body applications. The requirements for body fillers are different from facial fillers as they are applied for larger volume deficits, and experience greater mechanical stress. This study aims to fill this gap by analyzing the physicochemical and rheological properties of HA body fillers to guide clinical practice. - Source: PubMed
Fontenete SilviaAlfertshofer Michael - Understanding the molecular mechanisms that maintain protein homeostasis in cardiomyocytes is fundamental for the development of causal therapies for heart failure. Chaperones, the ubiquitin-proteasome system and autophagy are major regulators of cardiac homeostasis and are crucial for cardiomyocyte function and survival. In this context, myeloid leukaemia factor 2 (MLF2) emerged as a candidate of interest, as we found it overrepresented in protein aggregates in the hearts of mouse models of desmin-related cardiomyopathies (DRM), and it has also been suggested to be associated with dilated cardiomyopathy (DCM). Here, we identified αB-crystallin (CryAB), among other proteins, as a potential interaction partner of MLF2. Functionally, MLF2 was significantly upregulated in mouse models of heart failure and in two in vitro models of cardiomyocyte hypertrophy, and its overexpression resulted in attenuation of pro-hypertrophic gene expression. Taken together, these findings provide initial evidence supporting a role for MLF2 in regulating protein homeostasis and in modulating hypertrophic signalling in cardiomyocytes. - Source: PubMed
Publication date: 2025/12/30
Voran Jakob ChristophKilian Lucia SophieMartini SimoneLuzarowski MarcinNoormalal Marie IsabelMüller Oliver JosefRangrez Ashraf YusufFrank Derk - Osteosarcoma is the most common primary malignant bone cancer, characterized by a high incidence of lung metastasis and a lack of therapeutic targets. Here, by combining an in vivo CRISPR activation screen with the interactome of STUB1, a tumor suppressor in osteosarcoma, we identified that myeloid leukemia factor 2 (MLF2) promotes osteosarcoma metastasis. Mechanistically, MLF2 disrupted the interaction between BiP and IRE1α, thereby activating the IRE1α/XBP1-S-MMP9 axis. The E3 ligase STUB1 ubiquitinated MLF2 at Lys119 and targeted it for proteasomal degradation, whereas PIM3-mediated phosphorylation of MLF2 at Ser65 enhanced its stabilizing interaction with USP21. Our findings demonstrate that the PIM3/MLF2 axis is a critical regulator of osteosarcoma lung metastasis. We propose PIM3 as a potential therapeutic target for patients with osteosarcoma lung metastasis. - Source: PubMed
Publication date: 2025/10/15
Zeng CuilingWang XinZhong JinkunZhang YuDeng JuLiu WenqiangChen WeixuanYu XinhaoLin DianZhang RuhuaWang ShangLao JianpeiZhao QiZhong LiKang TiebangLiao Dan - [This corrects the article DOI: 10.1002/mlf2.12045.]. - Source: PubMed
Publication date: 2025/04/04
- Aberrant biomolecular condensates are implicated in multiple incurable neurological disorders, including Amyotrophic Lateral Sclerosis (ALS), Frontotemporal Dementia (FTD), and DYT1 dystonia. However, the role of condensates in driving disease etiology remains poorly understood. Here, we identify myeloid leukemia factor 2 (MLF2) as a disease-agnostic biomarker for phase transitions, including stress granules and nuclear condensates associated with dystonia. Exploiting fluorophore-derivatized MLF2 constructs, we developed a high-content platform and computational pipeline to screen modulators of NE condensates across chemical and genetic space. We identified RNF26 and ZNF335 as protective factors that prevent the buildup of nuclear condensates sequestering K48-linked polyubiquitinated proteins. Chemical screening identified four FDA-approved drugs that potently modulate condensates by resolving polyubiquitinated cargo and MLF2 accumulation. Our exploratory integrated chemical-genetics approach suggests that modulation of zinc, and potentially autophagy and oxidative stress, is critical for condensate modulation and nuclear proteostasis, offering potential therapeutic strategies for neurological disorders. Application of our platform to a genome-wide CRISPR KO screen identified strong enrichment of candidate genes linked to primary microcephaly and related neurodevelopmental disorders. Two hypomorphic microcephaly-associated alleles of ZNF335 failed to rescue nuclear condensate accumulation in ZNF335 KO cells, suggesting that aberrant condensates and impaired nuclear proteostasis may contribute to the pathogenesis of microcephaly. - Source: PubMed
Publication date: 2025/06/08
Poch DylanMukherjee ChandrayeeMallik SunandaTodorow VanessaKuiper E F ElsienaDhingra NaliniSurovtseva Yulia VSchlieker Christian