Concentrated polyclonal antibodies DFF_45
- Known as:
- Concentrated pab antibodies DFF_45
- Catalog number:
- RP138-05
- Product Quantity:
- 0.5ml
- Category:
- -
- Supplier:
- Diagnostic Biosystems
- Gene target:
- Concentrated polyclonal antibodies DFF_45
Related genes to: Concentrated polyclonal antibodies DFF_45
- Gene:
- DFFA NIH gene
- Name:
- DNA fragmentation factor subunit alpha
- Previous symbol:
- -
- Synonyms:
- DFF-45, DFF45, ICAD, DFF1
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-27
- Date modifiied:
- 2016-10-05
Related products to: Concentrated polyclonal antibodies DFF_45
Related articles to: Concentrated polyclonal antibodies DFF_45
- OBJECTIVE: Breast cancer continues to be a major contributor to cancer-associated deaths among the female population globally. This study aims to investigate the functional role, underlying mechanisms, and clinical relevance of Cell death-inducing DFFA-like effector C (CIDEC) in breast cancer pathogenesis. METHODS: Integrated bioinformatics analysis of three gene expression datasets identified hub genes via protein-protein interaction network and multiple machine learning algorithms. The tumor-suppressive effects of CIDEC were evaluated in vitro using breast cancer cell lines by assessing viability, proliferation, migration, invasion, and apoptosis, and in vivo via a xenograft model. Mitochondrial function, autophagy, and the cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) signaling pathway were assessed using a pathway agonist and an autophagy inhibitor. RESULTS: A marked reduction in CIDEC expression was observed in breast cancer tissues and cellular models. CIDEC effectively curtailed tumor progression by impeding proliferation, migration, and invasive capacity, coupled with the induction of apoptotic cell death. Mechanistically, CIDEC impaired mitochondrial fitness, characterized by reduced adenosine triphosphate (ATP) production, dissipated mitochondrial membrane potential, and elevated reactive oxygen species. Concurrently, CIDEC blocked protective autophagy. These effects were mediated through the suppression of the cGMP/PKG pathway. Activating this pathway with 8-Br-cGMP reversed the tumor-suppressive phenotypes and mitochondrial dysfunction induced by CIDEC, whereas inhibiting autophagy attenuated this rescue. CONCLUSION: Our findings demonstrate that CIDEC functions as a novel tumor suppressor in breast cancer by disrupting mitochondrial fitness and inhibiting protective autophagy via the cGMP/PKG pathway. The CIDEC-cGMP/PKG axis represents a promising therapeutic target for breast cancer intervention. CLINICAL TRIAL NUMBER: Not applicable. - Source: PubMed
Publication date: 2026/04/20
Jin XuchuLiu YuZheng XinyuHe Yangke - Glaucoma trabecular meshwork (GTM) cells cultured in vitro retain many characteristics of their in situ phenotype. Here, we used isobaric tandem mass tags (TMTpro) to label peptides from glaucomatous and non-glaucomatous TM (NTM) cells to identify differentially regulated proteins. Confluent NTM (n = 5) and GTM (n = 5) cells were lysed, proteins were trypsin digested, and peptides were labeled with 18-plex TMTpro. TMT-labeled peptides were fractionated on an Orbitrap Fusion mass spectrometer and data were processed using the PAW/Comet pipeline and EdgeR with Benjami–Hochberg multiple correction testing. Isobaric multiplexed quantitative proteomics identified 206 proteins that were significantly (FDR < 0.1) upregulated in GTM cells, 42 proteins that were downregulated, with 5270 non-candidates. Significant regulated pathways included extracellular matrix (DCN, COL4A1, CHI3L1), Wnt signaling (FZD1, FZD7, GSK3B), cytoskeletal regulation (ROCK2, MSN, TPM2, VIM, NF2), protein degradation (USP9X, LAMP1, SYNV1, UBE2L3), and nuclear proteins (LMNA, DFFA, CHMP3, RAD21). Western immunoblotting studies confirmed the TMTpro data. Immunofluorescence showed that the SNX7-stained nucleoli of GTM cells were significantly (p < 0.05) larger, and the DIAPH2 immunostaining was more distended into the cytosol than in NTM cells. This study identified many significantly regulated proteins in cultured GTM cells, and the results revealed several new avenues for developing clinical therapies for glaucoma patients. - Source: PubMed
Publication date: 2026/03/18
Holden PaulSun Ying YingZientek KeithWilmarth Phillip AReddy Ashok PKeller Kate E - In colorectal carcinoma (CRC), 5-fluorouracil (5-FU) remains the cornerstone of adjuvant systemic therapy, with folic acid (FA) serving as an essential adjunct. Expression of genes related to the metabolism and action of 5-FU and FA can be influenced by patient- and tumor-specific biological factors. In this study, we explore differential gene expression profiles of 180 genes representing 14 different gene sets associated with different 5-FU and FA metabolism processes, at both gene and pathway levels across clinical and molecular subgroups. In 71 patients with CRC, paired tumors and normal colonic tissues were analyzed. In CRC tissue, several gene sets (including Cell Cycle Checkpoint, Oxidative Stress Response, and Signaling Pathway, etc.) were upregulated, while three gene sets (Apoptotic, Tumor Suppressor, and Endoplasmic Reticulum Stress) were downregulated. Kirsten rat sarcoma virus (), tumor protein p53 (), and microsatellite instability (MSI) status impacted gene expression across molecular subgroups. At the individual gene level, among cell cycle genes, the BUB3 mitotic checkpoint protein () was upregulated in MSI tumors compared to MSS, whereas SMAD family member 4 () was downregulated in MSS tumors compared to MSI. DNA fragmentation factor alpha () was downregulated in MSI and upregulated in MSS. Notably, thymidylate synthetase () was more upregulated in MSI tumors (1.65-fold; 95% CI: 1.27-2.13) compared to MSS (1.19-fold; 95% CI: 1.02-1.39). Dysregulation of these genes across these factors will broaden our understanding of 5-FU-based treatment in CRC. Furthermore, targeting dysregulated pathways could form the basis for improved precision therapies tailored to CRC subtypes. - Source: PubMed
Publication date: 2025/11/26
Islam Muhammad RafiqulJasmine FarzanaVasiljevs DaniilRaza MarufAlmazan ArmandoAhsan HabibulKibriya Muhammad G - Excessive lipolysis and inflammatory response are critically involved in the pathogenesis of ketosis in periparturient dairy cows. Evidence has been growing for participation of the growth hormone (GH) in the metabolic regulation of adipose tissue. However, the potential role of GH in promoting lipolysis and proinflammatory signaling activation in bovine adipocytes remains to be elucidated. The objective of this study was to investigate the regulatory effects of GH on the lipolysis and inflammatory response of bovine adipocytes. Subcutaneous adipose tissue and blood samples were collected from 10 healthy cows (blood BHB concentration <1.2 mM) and 10 cows with clinical ketosis (CK; blood BHB concentration >3.0 mM). For in vitro experiments, adipocytes were isolated from healthy Holstein cows. Differentiated adipocytes were used for (1) treatment with 0, 5, 10, or 15 ng/mL of GH for 8 h, or 15 ng/mL of GH for 0, 4, 8 or 12 h; (2) co-treatment with 15 ng/mL GH and 0.1 ng/mL tumor necrosis factor α (TNF-α); (3) pretreatment with 10 μM BAY 11-7082, a nuclear factor kappa B (NF-κB) inhibitor, and then treatment with 15 ng/mL GH. The CK cows displayed higher serum GH concentration. The protein abundance of phosphorylated lipolysis-limiting enzyme hormone sensitive lipase (HSL) was higher and mRNA abundance of lipid droplet coating proteins cell death-inducing DFFA-like effector c and perilipin 1 was lower in adipose tissue of CK cows versus healthy cows. The protein abundance of phosphorylated inhibitor of kappa B α (IκBα) and NF-κB, mRNA abundance of proinflammatory cytokines TNFA, NLR family pyrin domain containing 3 (NLRP3), IL-18 (IL18), caspase 1 (CASP1) and IL-1B (IL1B), and the activity of caspase 1 were greater in adipose tissue of CK cows, but protein abundance of IκBα was lower. In bovine adipocytes, GH induced lipolysis and inflammatory response, as evidenced by increased glycerol content in the supernatant and decreased cellular triglyceride content, as well as elevated phosphorylation levels of IκBα and NF-κB, decreased protein abundance of IκBα, upregulated mRNA abundance of TNFA, NLRP3, IL18, CASP1, and IL1B, and enhanced caspase 1 activity. Furthermore, TNF-α exacerbated GH-induced lipolysis and inflammation, whereas inhibition of NF-κB signaling pathway partially reverses these metabolic alterations of GH-treated adipocytes. These findings suggested that GH promote lipolysis in bovine adipocytes by activating inflammatory pathways. - Source: PubMed
Publication date: 2025/12/13
Gao XinxingYu HaoShi ZhaoxinSong ChenyangFang ZhiyuanGao WenwenLei LinSong YuxiangLi XinweiDu XiliangLiu Guowen - The causes of pelvic organ prolapse (POP) recurrence are sufficiently understood. Few studies have investigated the key genes of the recurrence of POP. In the present study, we screened the hub genes responsible for the recurrence of POP. The GSE28660 gene expression dataset contained microarray data of 4 recurrent POP and 4 primary POP uterosacral ligaments. We used the online gene expression omnibus microarray expression profiling dataset to identify differentially expressed genes. Further analyses of functional enrichment and protein-protein interaction networks (PPIs) were conducted, and key modules were identified. In the next step, we used the CIBERSORT algorithm to investigate differences in immune cell infiltration between recurrent and primary POP tissues. A total of 84 upregulated genes and 32 downregulated genes were identified. DNA microarray analysis of the human genome identified 116 genes associated with recurrence POP, and 2 hub genes, including cell death-inducing DFFA-like effector (CIDEA) and hemoglobin subunit delta (HBD), may contribute to the pathogenesis of recurrence POP, potentially providing diagnostic and therapeutic value. - Source: PubMed
Liu WenhuaZhang Yue