Ask about this productRelated genes to: FLII antibody
- Gene:
- FLII NIH gene
- Name:
- FLII actin remodeling protein
- Previous symbol:
- -
- Synonyms:
- FLI, FLIL, Fli1, MGC39265
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-11
- Date modifiied:
- 2019-01-21
- Gene:
- LRRFIP1 NIH gene
- Name:
- LRR binding FLII interacting protein 1
- Previous symbol:
- -
- Synonyms:
- FLAP-1, FLIIAP1, TRIP, GCF-2, HUFI-1
- Chromosome:
- 2q37.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-15
- Date modifiied:
- 2016-06-20
Related products to: FLII antibody
Related articles to: FLII antibody
- BACKGROUND: Colorectal cancer (CRC) liver metastasis is a major factor affecting the prognosis of advanced CRC. Tumor-associated macrophages (TAMs), play a crucial role in CRC progression and metastasis by influencing the EMT of tumor cells. LRR binding FLII interacting protein 1, an epigenetic regulatory gene, a cancer-associated gene in a comprehensive analysis of human genome sequences; however, its role in CRC TAMs has not been elucidated. METHODS: We explored the expression and mechanism of action of LRRFIP1 in TAMs by single-cell transcriptome database analysis, immunostaining, flow cytometry, Western blotting, real-time quantitative PCR, enzyme-linked immunosorbent assay, and Transwell assay. Tumor growth and liver metastasis were examined in vivo. RESULTS: After knock down LRRFIP1 in TAMs in vitro, M2 phenotype and related cytokine expression were suppressed, whereas the promotion of CRC cell growth, migration, and invasion was inhibited. Interfering with LRRFIP1 did not further inhibit the TAMs phenotype or CRC progression after application of PI3K inhibitors or TGF-β receptor inhibitors. CONCLUSIONS: LRRFIP1 induces M2-like macrophage polarization via the PI3K/AKT signaling pathway, contributing to colorectal cancer progression. - Source: PubMed
Publication date: 2026/01/29
Mu SilongZhang ShuominWang MaihuanYuan XinpuZou GuijunZhang ChaojunCao Zhen - To investigate the biological functions of the transcription factor LRR binding FLII interacting protein 1 (LRRFIP1) in white adipocyte differentiation (WAD) and elucidate the underlying molecular regulatory mechanisms involved. - Source: PubMed
Publication date: 2025/11/12
Zhou LeiJiao YuwenXue JiamingZhan XiaoqiangWang DongmeiTang Liming - The obligate intracellular pathogen, , establishes an intracellular niche within a host membrane-derived vacuole called the chlamydial inclusion. From within this inclusion, orchestrates numerous host-pathogen interactions, in part, by utilizing a family of type III secreted effectors, termed inclusion membrane proteins (Incs). Incs are embedded within the inclusion membrane, and some function to recruit host proteins to the inclusion. Two such recruited host proteins are eucine ich epeat lightless-1 nteracting rotein 1 (LRRF1/LRRFIP1) and its binding partner Flightless 1 (FLI1/FLII). Previously, LRRF1 has been shown to interact with Inc protein Ct226/CTL0478. This is the first study to examine interactions of FLI1 with candidate Incs or with LRRF1 during infection. We hypothesized that FLI1 recruitment to the inclusion would be dependent on LRRF1 localization. We demonstrated that FLI1 co-immunoprecipitated with Ct226 but only in the presence of LRRF1. Furthermore, FLI1 localized to the inclusion when LRRF1 was depleted via small interfering RNA, suggesting that FLI1 may have an alternative recruitment mechanism. We further developed a series of CRISPRi knockdown and complementation strains in serovar L2 targeting ct226 and co-transcribed candidate Incs, ct225 and ct224. Simultaneous knockdown of ct226, ct225, and ct224 prevented localization of both FLI1 and LRRF1 to the inclusion, and only complementation of ct226 restored their localization. Thus, we demonstrated Ct226 is critical for FLI1 and LRRF1 localization to the inclusion. Our results also indicate an LRRF1-independent localization mechanism for FLI1, which likely influence their mechanism(s) of action during chlamydial infection.IMPORTANCE is a leading cause of both bacterial sexually transmitted infections and preventable infectious blindness worldwide. As an obligate intracellular pathogen, has evolved multiple ways of manipulating the host to establish a successful infection. As such, it is important to understand host-chlamydial protein-protein interactions as these reveal strategies that uses to shape its intracellular environment. This study looks in detail at interactions of two host proteins, FLI1 and LRRF1, during chlamydial infection. Importantly, the series of CRISPR inference knockdown and complement strains developed in this study suggest these proteins have both independent and overlapping mechanisms for localization, which ultimately will dictate how these proteins function during chlamydial infection. - Source: PubMed
Publication date: 2024/10/15
Sturd Natalie AKnight Lindsey AWood Macy GDurham LegacyOuellette Scot PRucks Elizabeth A - Chronic inflammatory diseases are associated with hematopoietic lineage bias, including neutrophilia and anemia. We have recently identified that the canonical inflammasome mediates the cleavage of the master erythroid transcription factor GATA1 in hematopoietic stem and progenitor cells (HSPCs). We report here that genetic inhibition of Nlrp1 resulted in reduced number of neutrophils and increased erythrocyte counts in zebrafish larvae. We also found that the NLRP1 inflammasome in human cells was inhibited by LRRFIP1 and FLII, independently of DPP9, and both inhibitors regulated hematopoiesis. Mechanistically, erythroid differentiation resulted in ribosomal stress-induced activation of the ZAKα/P38 kinase axis which, in turn, phosphorylated and promoted the assembly of NLRP1 in both zebrafish and human. Finally, inhibition of Zaka with the FDA/EMA-approved drug Nilotinib alleviated neutrophilia in a zebrafish model of neutrophilic inflammation and promoted erythroid differentiation and GATA1 accumulation in K562 cells. In conclusion, our results reveal that the NLRP1 inflammasome regulates hematopoiesis and pave the way to develop novel therapeutic strategies for the treatment of hematopoietic alterations associated with chronic inflammatory and rare diseases. - Source: PubMed
Publication date: 2023/09/07
Rodríguez-Ruiz LolaLozano-Gil Juan MNaranjo-Sánchez ElenaMartínez-Balsalobre ElenaMartínez-López AliciaLachaud ChristopheBlanquer MiguelPhung Toan KGarcía-Moreno DianaCayuela María LTyrkalska Sylwia DPérez-Oliva Ana BMulero Victoriano - Children born preterm are at heightened risk of neurodevelopmental impairments, including Autism Spectrum Disorder (ASD). The placenta is a key regulator of neurodevelopmental processes, though the precise underlying molecular mechanisms remain unclear. Here, we employed a multi-omic approach to identify placental transcriptomic and epigenetic modifications related to ASD diagnosis at age 10, among children born preterm. Working with the extremely low gestational age (ELGAN) cohort, we hypothesized that a pro-inflammatory placental environment would be predictive of ASD diagnosis at age 10. Placental messenger RNA (mRNA) expression, CpG methylation, and microRNA (miRNA) expression were compared among 368 ELGANs (28 children diagnosed with ASD and 340 children without ASD). A total of 111 genes displayed expression levels in the placenta that were associated with ASD. Within these ASD-associated genes is an ASD regulatory complex comprising key genes that predicted ASD case status. Genes with expression that predicted ASD case status included Ewing Sarcoma Breakpoint Region 1 (EWSR1) (OR: 6.57 (95% CI: 2.34, 23.58)) and Bromodomain Adjacent To Zinc Finger Domain 2A (BAZ2A) (OR: 0.12 (95% CI: 0.03, 0.35)). Moreover, of the 111 ASD-associated genes, nine (8.1%) displayed associations with CpG methylation levels, while 14 (12.6%) displayed associations with miRNA expression levels. Among these, LRR Binding FLII Interacting Protein 1 (LRRFIP1) was identified as being under the control of both CpG methylation and miRNAs, displaying an OR of 0.42 (95% CI: 0.17, 0.95). This gene, as well as others identified as having functional epimutations, plays a critical role in immune system regulation and inflammatory response. In summary, a multi-omic approach was used to identify functional epimutations in the placenta that are associated with the development of ASD in children born preterm, highlighting future avenues for intervention. - Source: PubMed
Publication date: 2023/03/20
Freedman Anastasia NClark JeliyahEaves Lauren ARoell KyleOran AliKoval LaurenRager JuliaSantos Hudson PKuban KarlJoseph Robert MFrazier JeanMarsit Carmen JBurt Amber AO'Shea T MichaelFry Rebecca C