CFLAR, 1-480aa, Human, E.coli
- Known as:
- Cellular FLICE-like inhibitory protein, 1-480aa, Human, E.coli
- Catalog number:
- ATGP1195
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- CFLAR 1-480aa Human .coli
Related genes to: CFLAR, 1-480aa, Human, E.coli
- Gene:
- CFLAR NIH gene
- Name:
- CASP8 and FADD like apoptosis regulator
- Previous symbol:
- CASP8AP1
- Synonyms:
- CASH, Casper, CLARP, FLAME, FLIP, I-FLICE, MRIT, c-FLIP, cFLIP
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2019-02-25
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
Related products to: CFLAR, 1-480aa, Human, E.coli
Related articles to: CFLAR, 1-480aa, Human, E.coli
- Glaesserella parasuis (G. parasuis) is an important opportunistic pathogen that poses a threat to the swine industry, and the induction of host cell apoptosis is one of the key pathogenic mechanisms by which G. parasuis invades and damages the host. Long non-coding RNAs (lncRNAs) exert diverse and crucial biological functions in cells. Maternally expressed gene 3 (MEG3), a lncRNA widely involved in cell proliferation, apoptosis, and immune responses, has been demonstrated to be associated with G. parasuis infection. However, the function and mechanism of MEG3 in regulating G. parasuis-induced apoptosis remain unclear. In this study, we found that in the porcine alveolar macrophage cell line 3D4/21, MEG3 interacts with interleukin enhancer-binding factor 3 (ILF3) and negatively regulates the protein expression of ILF3 in the nucleus. Functional analysis showed that ILF3 suppresses G. parasuis-induced apoptosis of 3D4/21 cells, whereas MEG3 participates in regulating this apoptotic process through its interaction with ILF3. Further mechanistic studies revealed that MEG3 acts as a molecular scaffold to recruit the E3 ubiquitin ligase MDM2, enhances the interaction between MDM2 and ILF3, and thereby promotes the ubiquitination and degradation of ILF3. Moreover, ILF3 binds to the promoter of the anti-apoptotic gene CFLAR to facilitate its transcription, whereas MEG3 inhibits ILF3-mediated transcriptional activation of CFLAR, consequently regulating G. parasuis-induced apoptosis of 3D4/21 cells. This study reveals a novel mechanism by which MEG3 regulates G. parasuis-induced apoptosis of 3D4/21 cells via the MDM2/ILF3/CFLAR axis. These findings provide new insights into elucidating the molecular pathogenic mechanisms of G. parasuis. - Source: PubMed
Publication date: 2026/09/23
Jia YongchaoLi NaWang HaoranYin RonglanShen AoboZeng FanhuaLiu XueqianLi JiayingZhou YuanyuanYuan JingYin Ronghuan - Cell death during late-stage culture remains a major limitation in mammalian manufacturing processes for antibody therapeutics, constraining yield and process robustness. Here, we identified the predominant apoptotic signalling axis associated with culture decline in Chinese hamster ovary (CHO) cells and engineering against it. Recombinant CHO lines were engineered to overexpress BCL-2 (intrinsic pathway and benchmark control), CFLAR (death receptor pathway regulator), or TPT1 (a multifunctional stress-response protein). Apoptosis profiling across fed-batch cultures indicated that viability loss is predominantly associated with intrinsic pathway activation, characterised by increased cleavage of caspase-9, caspase-7 and caspase-3, with minimal activation of caspase-8. In batch and fed-batch studies, CFLAR and TPT1 improved late-stage viability and extended culture lifespan relative to the control, with TPT1 providing the most consistent benefit and outperforming BCL-2 in overall process performance. Under apoptosis challenges, including chemical induction, pro-apoptotic BAK overexpression and caspase 3 activation, TPT1-expressing cells maintained higher viability, decreased apoptosis and attenuated caspase 3 activation. Finally, TPT1 overexpression was transferred to industrially relevant CHO DG44 production platforms expressing monoclonal and bispecific antibodies and improved culture longevity and titres in both formats, without altering cell-specific productivity and N-glycan profile. TPT1 also presented similar behaviour to a BAK/BAX double knockout on viability and exceeded it on growth and titre, and combining the two gave no further gain in unfed batch culture. TPT1 overexpression therefore offers a single-cassette route to longer culture and high volumetric output inCHO-based bioprocesses. - Source: PubMed
Publication date: 2026/08/31
Bravo-Venegas JavierBetts ZeynepKalsi DevikaPybus Leon POrellana Camila AAltamirano ClaudiaDickson Alan JTorres Mauro - Although copy number variants (CNVs) represent well-established genetic contributors to schizophrenia (SCZ), their role in bipolar disorder (BD), especially within non-European ancestries, has been inadequately explored. We evaluated the genome-wide load of rare CNVs, encompassing deletions and duplications, in a Han Chinese sample of 3915 BD cases and 7820 ethnically matched controls. We observed a marked overrepresentation of rare deletions in BD patients relative to controls, with affected genes showing enrichment in neural signaling and dosage-dependent networks, indicating that haploinsufficiency in neurodevelopmental loci could underlie a central etiological pathway in BD. Among the 12 previously reported CNV loci from European cohorts, only deletions at 3q29 and 15q11.2 exhibited robust associations with BD susceptibility in Han Chinese individuals. Through genome-wide, gene-centric CNV association testing, we uncovered novel BD-linked loci, including deletions spanning GLIS2 and PAM16 at 16p13.3, GRID2IP at 7p22.1, and CFLAR at 2q33.1, alongside a duplication affecting ZNF878 and ZNF844 at 19p13.2. These disrupted genes are chiefly implicated in neuronal maturation, synaptic modulation, and mitochondrial dynamics. This work delivers the most thorough delineation of BD-associated CNVs in Han Chinese to date, underscoring the imperative for ancestry-inclusive research to comprehensively unravel psychiatric genomics and unveiling fresh mechanistic perspectives on BD etiology. - Source: PubMed
Publication date: 2026/08/27
Wu YongLi XiangyuSun YaoyaoZhang ChuyiSun PingHui LiZhao YingFeng XiaoyangWang BaokunYang JianzhongZhang NanYuan JingJiang HongyanCheng YuqiMa SimengGong QianYin XuyuanYang YongfengLi WenqiangLv LuxianZhou DongshengLi XingxingChen XiaogangZhang ChenSong XueqinTang WenxinLiu ZhongchunShi YongyongXiao XiaoYue WeihuaLi ZhiqiangLi Ming - Cervical cancer ranks as the fourth most prevalent malignancy among women across the world. Tanshinone I (Tan I), a principal bioactive component of has demonstrated broad therapeutic potential in various cancers, yet its mechanism of action against cervical cancer remains unclear. In this study, we demonstrate that Tan I exerts potent anti-cervical cancer effects by inhibiting proliferation and inducing apoptosis in SiHa and HeLa cervical cancer cell lines. Mechanistically, Tan I may target RSF1, as evidenced by the finding that overexpression of RSF1 attenuated Tan I's inhibitory effect, whereas RSF1 knockdown enhanced its efficacy. Through RSF1 targeting, Tan I suppresses the NF-κB signaling pathway and downregulates key anti-apoptotic genes, including , , , and . Moreover, Tan I enhances the cytotoxic activity of carboplatin when used in combination. Together, these results indicate that Tan I inhibits cervical cancer cell growth by targeting RSF1 and suppressing the NF-κB pathway, supporting its further development as a promising therapeutic candidate against cervical cancer. - Source: PubMed
Publication date: 2026/08/12
Shen YuanLu ShunZhao QiannaCui TongtongCui HongqianCui ZhenwuShan LinlinGuo ChaoShi Lei - This study aimed to investigate the selective anticancer activity of the curcumin analog PAC (3,5-Bis-4-hydroxy-3-methoxybenzylidene)-N-methyl-4-piperidone). Normal gingival epithelial cells (GECs), cancerous gingival cells (Ca9-22) and tongue squamous carcinoma cells (CAL27) were exposed to increasing concentrations of PAC (0-10 µM) for 24 h. Cell viability and cytotoxicity were evaluated using MTT and LDH assays, while apoptosis and caspase activation were analyzed by Annexin V/PI staining and flow cytometry. Gene-expression profiling was performed using RT Profiler PCR arrays. PAC significantly inhibited Ca9-22 and CAL27 cell proliferation in a concentration-dependent manner, with an IC value of 5 µM, while exerting no noticeable cytotoxic effects on normal GEC. PAC treatment induced significant early and late apoptosis associated with increased caspase activity in both oral cancer cell lines. Transcriptomic analyses revealed extensive modulation of apoptosis-related genes. In Ca9-22 cells, PAC predominantly suppressed anti-apoptotic and survival-associated genes, including BCL2, BIRC3, BIRC5, XIAP, CFLAR, and NFKB1. In contrast, CAL27 cells exhibited a more pronounced pro-apoptotic transcriptional profile characterized by upregulation of TP53, APAF1, CASP1, BID, and TNF. Gene interaction network analyses further demonstrated that PAC targets highly interconnected apoptotic signaling pathways. Collectively, these findings demonstrate that PAC exerts potent selective anticancer activity against OSCC cells through modulation of intrinsic and extrinsic apoptotic pathways. These results further support the therapeutic potential of PAC as a promising multitarget candidate for oral cancer treatment. - Source: PubMed
Publication date: 2026/06/23
Benchekroun SaraHammache MeriemChandad FatihaAlmutairi Mikhlid HDaich AdamBadwelan MohammedRouabhia MahmoudSemlali Abdelhabib