RASSF7 antibody - C - terminal region (OAAB12372)
- Known as:
- RASSF7 (anti-) - C - terminal region (OAAB12372)
- Catalog number:
- oaab12372
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RASSF7 antibody - terminal region (OAAB12372)
Related genes to: RASSF7 antibody - C - terminal region (OAAB12372)
- Gene:
- RASSF7 NIH gene
- Name:
- Ras association domain family member 7
- Previous symbol:
- C11orf13
- Synonyms:
- HRC1, HRAS1
- Chromosome:
- 11p15.5
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-18
- Date modifiied:
- 2016-01-29
Related products to: RASSF7 antibody - C - terminal region (OAAB12372)
Related articles to: RASSF7 antibody - C - terminal region (OAAB12372)
- The neurodevelopmental toxicity of bisphenol A (BPA) and its substitutes has garnered significant attention. However, the association between two widely detected environmental contaminants-BPAF and BPB-and adolescent depression, along with their underlying mechanisms, remain largely unclear. Here, we established a prenatal BPB/BPAF exposure animal model and demonstrated that such exposure induces depression- and anxiety-like behaviors in weanling male offspring. Through RNA sequencing of cortical tissues, combined with screening of depression-associated transcription factors (TFs), functional enrichment analysis of target genes, and identification of hub genes, we revealed that BPB and BPAF drive disease progression via distinct transcriptional regulatory networks and biological processes. Specifically, BPB significantly downregulate the TFs Lhx8 and Foxp1, targeting hub genes (e.g., Alb, Apoa1, Apoa2, Fga, Serpina1b, Fos, Rassf6, Rassf10, Rassf7, Moap1) to disrupt neuropeptide-, synapse-, transcription- related biological processes. In contrast, BPAF significantly upregulate the TF Neurod1, which modulate hub genes (e.g., Rpl26, Mrpl3,Rpl35, Mrpl1, Kcnd3) involved in neuronal cell body and cerebral cortex development. Molecular docking further confirmed potential binding interactions between BPB and Lhx8/ Foxp1, as well as BPAF and Neurod1, mediated by hydrogen bonding or hydrophobic interactions. These findings demonstrate that BPB and BPAF induce depression-like behavior in male offspring through compound-specific disruption of transcriptional networks, which alter neurodevelopmental pathways, potentially due to their divergent binding affinities to distinct TFs. This research offers new perspectives on the neurodevelopmental toxicity associated with BPA alternatives, offering critical implications for risk assessment and therapeutic targeting of BPAF/BPB-related neuropsychiatric disorders. - Source: PubMed
Publication date: 2025/09/11
Chen NannanLiu YuetongZhouguo YiranCai XueyiPan XinyiGuo RuiYan Wei - In the tumor microenvironment (TME), tumor associated macrophages (TAMs) often exhibit a preference for M2-like phenotype, which supports tumor progression under hypoxia. The underlying mechanisms driving the behavior of hypoxic TAMs are highly complex. Recently, exosomal long non-coding RNAs (lncRNAs) derived from non-cancerous cells within TME have attracted more attention from researchers. In the present study, we investigated the function of exosomal lncRNA MIR210HG derived from hypoxic TAMs in triple negative breast cancer (TNBC). Results showed that MIR210HG was significantly upregulated in hypoxic TAMs, their exosomes, and exosomes-treated TNBC cells. When MIR210HG was suppressed, the expression of M2-polarization markers and proteins associated with the PI3K/Akt/mTOR pathway in hypoxic TAMs was notably inhibited. Moreover, the suppression of TAM-derived exosomal MIR210HG effectively inhibited the migration, invasion and vasculogenic mimicry (VM) formation of TNBC cells. Notably, dual inhibition of both exosomal and endogenous MIR210HG in tumor cells synergistically restricted TNBC metastasis of in vivo. Mechanistically, we elucidated that MIR210HG promoted the malignant phenotypes of TNBC by upregulating the expression of HIF-1α protein, which in turn initiated RASSF7 transcription, resulting in the promotion of epithelial-mesenchymal transition (EMT) process. Collectively, our results identified MIR210HG as a key molecule mediating exosome-based communication from hypoxic TAMs to TNBC cells and revealed its pro-metastatic role, Consequently, MIR210HG emerges as a highly promising therapeutic target of TNBC. - Source: PubMed
Publication date: 2025/08/29
Feng LiyaWang YuanxinWang XiangyueLi BaochanLiu YifanZhang WanyingJi JianboShao LijunGuo Xiuli - To investigate the clinical value of serum autoantibodies in the screening and diagnosis of gastric cancer. - Source: PubMed
Publication date: 2025/02/01
Xiao KangjiaXie ChengxuanZhang YiKang MeihuaWang YanchunLi QingtianDong WenqianWang HaoWei HuaxingHu YanpingWang BaolongLu Renquan - - Source: PubMed
Publication date: 2022/04/26
Lu YaliLin YanZhang XiaoyangYan JunKong ZheZhang LuWang ChenjiHuang YanZhao ShiminLi Yao - Traffic-related air pollution (TRAP), a common exposure, potentially impacts pregnancy through altered placental function. We investigated associations between prenatal TRAP exposure and placental gene expression. - Source: PubMed
Publication date: 2023/05/14
Hussey Michael REnquobahrie Daniel ALoftus Christine TMacDonald James WBammler Theo KPaquette Alison GMarsit Carmen JSzpiro Adam AKaufman Joel DLeWinn Kaja ZBush Nicole RTylavsky FrancesZhao QiKarr Catherine JSathyanarayana Sheela