CFLAR & CASP10 Protein Protein Interaction Antibody Pair
- Known as:
- Cellular FLICE-like inhibitory protein & CASP10 Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0078
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CFLAR & CASP10 Protein Interaction Antibody Pair
Related genes to: CFLAR & CASP10 Protein Protein Interaction Antibody Pair
- Gene:
- CASP10 NIH gene
- Name:
- caspase 10
- Previous symbol:
- -
- Synonyms:
- MCH4
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-21
- Date modifiied:
- 2019-04-23
- 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
Related products to: CFLAR & CASP10 Protein Protein Interaction Antibody Pair
Related articles to: CFLAR & CASP10 Protein Protein Interaction Antibody Pair
- This paper studies the toxic effect of micron-sized quartz silica particles on primary human airway epithelial cells (AECs) and the molecular mechanism of its induction of apoptosis. Studies have found that micron-sized quartz silica particles cause AECs damage by activating cell apoptosis. By constructing a competitive endogenous RNA (ceRNA) network, it was identified that three circRNAs (hsa_circ_0052203, hsa_circ_0022429, hsa_circ_0052264) and four key miRNAs (hsa-miR-4646-5p, hsa-miR-150-3p, hsa-miR-6798-3p, hsa-miR-6756-5p) play key roles in regulating apoptosis. In addition, seven mRNAs (LMNB1, TP53AIP1, CASP10, BCL2, LMNB2, CFLAR and ITPR1) were significantly associated with the apoptosis. Functional enrichment analysis indicated that these genes were involved in biological processes such as nuclear lysis, hypoxia response and DNA damage. This study has for the first time revealed the role of the ceRNA network in the apoptosis of AECs induced by micron-sized quartz silica particles, providing new molecular targets and therapeutic ideas for the early pathogenesis of silicosis. - Source: PubMed
Publication date: 2025/08/14
Ma JiaziHan BingYang YongZhang YuCao MaoCao WenyueZhang WeiCheng MengjieCui GuanqunDu ZhongjunChen Shangya - Cell death pathway plays an important role in apoptosis, and corruption of this signaling pathway has been shown to participate in carcinogenesis. We aimed at determining whether genetic variants in CASP8, CASP10 and CFLAR influence the development and clinical outcomes of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). A hospital-based case-control study, including 600 HCC cases and 600 HBsAg positive controls without HCC, was conducted to assess the relationship between 11 tagging SNPs in CASP8, CASP10 and CFLAR and HBV-related HCC risk and prognosis in a Chinese Han population. Among the 11 polymorphisms, only CASP8 rs3834129 (-652 6N ins/del) modified HCC risk. Compared with CASP8 -652 insins genotype, the deldel (adjusted OR 0.717, 95% CI 0.553-0.930) and insdel (adjusted OR 0.731, 95% CI 0.554-0.964) genotypes had a significantly decreased HCC risk. Furthermore, this polymorphism was significantly associated with decreased portal vein tumor thrombosis (adjusted OR 0.554; P = 0.044) and reduced postoperative recurrence (adjusted OR 0.356; P < 0.001) of resected HCC. In addition, the multivariate analysis showed that the -652 6N ins/del polymorphism was significantly associated with improved overall survival and recurrence-free survival of resected HCC patients. The expression levels of CASP8 in HCC tumor tissues were significantly lower than those in paracancerous liver tissues, although no significant association between -652 6N ins/del genotypes and the expression levels of CASP8 were observed in these tissues. These results suggest that the CASP8 -652 6N ins/del polymorphism may play a protective role in the development, progression, and survival of HBV-related HCC among the Chinese Han population. - Source: PubMed
Liu FeiLi FuqiangLuo LimeiYang HantengWei YonggangWang WentaoYan LvnanWen TianfuYang JiayinLi Bo - Populations in north central China are at high risk for gastric cancers (GC), and altered FAS-mediated cell signaling and/or apoptosis may contribute to this risk. We examined the association of 554 single nucleotide polymorphisms (SNPs) in 53 Fas signaling-related genes using a pathway-based approach in 1758 GC cases (1126 gastric cardia adenocarcinomas (GCA) and 632 gastric noncardia adenocarcinomas (GNCA)), and 2111 controls from a genome-wide association study (GWAS) of GC in ethnic Chinese. SNP associations with risk of overall GC, GCA and GNCA were evaluated using unconditional logistic regressions controlling for age, sex and study. Gene- and pathway-based associations were tested using the adaptive rank-truncated product (ARTP) method. Statistical significance was evaluated empirically by permutation. Significant pathway-based associations were observed for Fas signaling with risk of overall GC (p = 5.5E-04) and GCA (p = 6.3E-03), but not GNCA (p= 8.1E-02). Among examined genes in the Fas signaling pathway, MAP2K4, FAF1, MAPK8, CASP10, CASP8, CFLAR, MAP2K1, CAP8AP2, PAK2 and IKBKB were associated with risk of GC (nominal p < 0.05), and FAF1 and MAPK8 were significantly associated with risk of both GCA and GNCA (nominal p< 0.05). Our examination of genetic variation in the Fas signaling pathway is consistent with an association of altered Fas signaling and/or apoptosis with risk of GC. As one of the first attempts to investigate a pathway-level association, our results suggest that these genes and the Fas signaling pathway warrant further evaluation in relation to GC risk in other populations. - Source: PubMed
Publication date: 2013/09/11
Hyland Paula LLin Shih-WenHu NanZhang HanWang LeminSu HuaWang ChaoyuDing TiTang Ze-ZhongFan Jin-HuQiao You-LinXiong XiaoqinWheeler WilliamGiffen CarolYu KaiYuenger JeffBurdett LaurieWang ZhaomingChanock Stephen JTucker Margaret ADawsey Sanford MFreedman Neal DGoldstein Alisa MAbnet Christian CTaylor Philip R - Chronic obstructive pulmonary disease (COPD) is a major global health problem. The etiology of COPD has been associated with apoptosis, oxidative stress, and inflammation. However, understanding of the molecular interactions that modulate COPD pathogenesis remains only partly resolved. We conducted an exploratory study on COPD etiology to identify the key molecular participants. We used information-theoretic algorithms including Context Likelihood of Relatedness (CLR), Algorithm for the Reconstruction of Accurate Cellular Networks (ARACNE), and Inferelator. We captured direct functional associations among genes, given a compendium of gene expression profiles of human lung epithelial cells. A set of genes differentially expressed in COPD, as reported in a previous study were superposed with the resulting transcriptional regulatory networks. After factoring in the properties of the networks, an established COPD susceptibility locus and domain-domain interactions involving protein products of genes in the generated networks, several molecular candidates were predicted to be involved in the etiology of COPD. These include COL4A3, CFLAR, GULP1, PDCD1, CASP10, PAX3, BOK, HSPD1, PITX2, and PML. Furthermore, T-box (TBX) genes and cyclin-dependent kinase inhibitor 2A (CDKN2A), which are in a direct transcriptional regulatory relationship, emerged as preeminent participants in the etiology of COPD by means of senescence. Contrary to observations in neoplasms, our study reveals that the expression of genes and proteins in the lung samples from patients with COPD indicate an increased tendency towards cellular senescence. The expression of the anti-senescence mediators TBX transcription factors, chromatin modifiers histone deacetylases, and sirtuins was suppressed; while the expression of TBX-regulated cellular senescence markers such as CDKN2A, CDKN1A, and CAV1 was elevated in the peripheral lung tissue samples from patients with COPD. The critical balance between senescence and anti-senescence factors is disrupted towards senescence in COPD lungs. - Source: PubMed
Publication date: 2012/07/19
Acquaah-Mensah George KMalhotra DeeptiVulimiri MadhulikaMcDermott Jason EBiswal Shyam - The effect of the B-cell chronic lymphocytic leukemia/lymphoma 11B gene (BCL11B) on human T-cell regulation remains unclear. To characterize the functions of BCL11B, recombinant BCL11B and BCL11B siRNA were transfected into human naive T cells to overexpress or knock down BCL11B expression, respectively. After BCL11B overexpression, the proliferation ability and the T-helper (Th) subset were increased, whereas no significant alteration in the expression pattern and clonality of the T-cell receptor Vβ subfamilies was observed. After BCL11B knockdown, a similar distribution of Vβ subfamilies was detected in the naive T cells; however, the proliferation capacity substantially decreased. Global gene expression profiling revealed that the dysregulated genes were mainly involved in T-cell activation and proliferation. BCL11B could selectively promote Th-cell differentiation because of increased CXCL10 and CXCL11 expression. BCL11B suppression may inhibit proliferation and induce apoptosis, which may relate to changes in the expression of CFLAR-CASP8-CASP10 in the mitochondrial pathways. In conclusion, BCL11B is required for T-cell survival; its overexpression could effectively increase the T-cell activation and proliferation abilities and Th-cell differentiation as well. - Source: PubMed
Publication date: 2012/03/07
Chen SiHuang XinChen ShaohuaYang LijianShen QiZheng HaitaoLi BoGrabarczyk PiotrPrzybylski Grzegorz KSchmidt Christian ALi Yangqiu