Ask about this productRelated genes to: NCBP2 antibody
- Gene:
- NCBP2 NIH gene
- Name:
- nuclear cap binding protein subunit 2
- Previous symbol:
- -
- Synonyms:
- NIP1, CBP20, Cbc2
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-17
- Date modifiied:
- 2015-11-09
- Gene:
- NCBP2AS2 NIH gene
- Name:
- NCBP2 antisense 2 (head to head)
- Previous symbol:
- NCBP2-AS2
- Synonyms:
- HIAR
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2013-05-17
- Date modifiied:
- 2019-03-07
Related products to: NCBP2 antibody
Related articles to: NCBP2 antibody
- Breast cancer (BC) accounts for approximately one-third of Cancer cases. It is responsible for nearly 16% of all cancer-related deaths among females. Increasing incidence and high mortality associated with BC has prompted the researchers to investigate the genetic and epigenetic mechanisms of the disease. - Source: PubMed
Publication date: 2025/10/09
Badr Eman A EAlashkar Hagar GEl-Rebey Hala SaidKhlosy Eman A EGhobashy Eman Abdel-RahimAbdelbary Hammed Mohamed - Microproteins, short functional peptides encoded by small genes, are emerging as critical regulators of cellular processes, yet their roles in mitochondrial function and neurodegeneration remain underexplored. In this study, we identify NCBP2-AS2 as an evolutionarily conserved mitochondrial microprotein with significant roles in energy metabolism and neurogenesis. Using a combination of cellular and molecular approaches, including CRISPR/Cas9 knockout models, stoichiometric co- immunoprecipitation, and advanced imaging techniques, we demonstrate that NCBP2-AS2 localizes to the inner mitochondrial space and interacts with translocase of the inner membrane (TIM) chaperones. These interactions suggest a role in ATPase subunit transport, supported by the observed reductions in ATPase subunit levels and impaired glucose metabolism in NCBP2-AS2-deficient cells. In zebrafish, NCBP2-AS2 knockout led to increased astroglial proliferation, microglial abundance, and enhanced neurogenesis, particularly under amyloid pathology. Notably, we show that NCBP2-AS2 expression is consistently downregulated in human Alzheimer's disease brains and zebrafish amyloidosis models, suggesting a conserved role in neurodegenerative pathology. These findings reveal a novel link between mitochondrial protein transport, energy metabolism, and neural regeneration, positioning NCBP2-AS2 as a potential therapeutic target for mitigating mitochondrial dysfunction and promoting neurogenesis in neurodegenerative diseases such as Alzheimer's disease. - Source: PubMed
Publication date: 2025/01/27
Popova StanislavaBhattarai PrabeshYilmaz ElanurLascu DanielaKuo Juo-HanErdem GizemCoban BasakMichling JitkaCosacak Mehmet IlyasTayran HuseyinKurth ThomasSchambony AlexandraBuchholz FrankGentzel MarcKizil Caghan - Ovarian cancer stem cells (OCSCs) are the main cause of relapse and drug resistance in patients with ovarian cancer. Anisomycin has been shown to be an effective antitumor agent, but its mechanism of action in ovarian cancer remains elusive. - Source: PubMed
Publication date: 2023/07/22
Ling LeleWen YichaoXiong YingLiu XinChen JuanLiu TeZhang Bimeng - Osteoporosis (OP) is a multifactorial disease influenced by genetic, epigenetic, and environmental factors. One of the main causes of the bone homeostasis alteration is inflammation resulting in excessive bone resorption. Long non-coding RNAs (lncRNAs), have a crucial role in regulating many important biological processes in bone, including inflammation. We designed our study to identify lncRNAs misregulated in osteoblast primary cultures derived from OP patients ( = 4), and controls (CTRs, = 4) with the aim of predicting possible RNA and/or protein targets implicated in this multifactorial disease. We focused on 84 lncRNAs regulating the expression of pro-inflammatory and anti-inflammatory genes and miRNAs. In silico analysis was utilized to predict the interaction of lncRNAs with miRNAs, mRNAs, and proteins targets. Six lncRNAs were significantly down-regulated in OP patients compared to controls: , , , , , and . Bioinformatic analyses identified HDCA2, PTX3, and FGF2 proteins as downstream targets of , and lncRNAs mediated by the interaction with miRNAs implicated in OP pathogenesis, including p. Altogether, these data open a new regulatory mechanism of gene expression in bone homeostasis and could direct the development of future therapeutic approaches. - Source: PubMed
Publication date: 2020/03/19
Centofanti FedericaSantoro MassimoMarini MarioVisconti Virginia VeronicaRinaldi Anna MariaCeli MonicaD'Arcangelo GiovannaNovelli GiuseppeOrlandi AugustoTancredi VirginiaTarantino UmbertoBotta Annalisa - The roles of concealed microproteins encoded by long noncoding RNAs (lncRNAs) are gradually being exposed, but their functions in tumorigenesis are still largely unclear. Here, we identify and characterize a conserved 99-amino acid microprotein named KRASIM that is encoded by the putative lncRNA NCBP2-AS2. KRASIM is differentially expressed in normal hepatocytes and hepatocellular carcinoma (HCC) cells and can suppress HCC cell growth and proliferation. Mechanistically, KRASIM interacts and colocalizes with the KRAS protein in the cytoplasm of human HuH-7 hepatoma cells. More importantly, the overexpression of KRASIM decreases the KRAS protein level, leading to the inhibition of ERK signaling activity in HCC cells. These results demonstrate a novel microprotein repressor of the KRAS pathway for the first time and provide new insights into the regulatory mechanisms of oncogenic signaling and HCC therapy. - Source: PubMed
Publication date: 2019/06/24
Xu WenliDeng BingLin PenghuiLiu ChangLi BinHuang QiaojuanZhou HuiYang JianhuaQu Lianghu