Recombinant HIV-I NEF Biotin conjugated
- Known as:
- Recombinant H. sapiens immunodeficiency virus-I NEF Biotin labelled
- Catalog number:
- REP0046
- Product Quantity:
- 100 mcg
- Category:
- -
- Supplier:
- DIATHEVA
- Gene target:
- Recombinant HIV- NEF Biotin conjugated
Related genes to: Recombinant HIV-I NEF Biotin conjugated
- Gene:
- CCNT1 NIH gene
- Name:
- cyclin T1
- Previous symbol:
- HIVE1
- Synonyms:
- CCNT, CYCT1
- Chromosome:
- 12q13.11-q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-29
- Date modifiied:
- 2018-02-13
- Gene:
- HIVEP2 NIH gene
- Name:
- human immunodeficiency virus type I enhancer binding protein 2
- Previous symbol:
- -
- Synonyms:
- MBP-2, HIV-EP2, MIBP1, ZAS2, Schnurri-2, ZNF40B
- Chromosome:
- 6q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-21
- Date modifiied:
- 2016-10-05
- Gene:
- KCND3 NIH gene
- Name:
- potassium voltage-gated channel subfamily D member 3
- Previous symbol:
- SCA22, SCA19
- Synonyms:
- Kv4.3, KSHIVB
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-05
- Date modifiied:
- 2019-04-23
Related products to: Recombinant HIV-I NEF Biotin conjugated
Related articles to: Recombinant HIV-I NEF Biotin conjugated
- Elevated brain pro-inflammatory cytokines are found in the midbrain of about 50% of the people with schizophrenia, and increased transcription factor nuclear factor-kappa B (NF-κB) could be responsible. Here, we tested if NF-κB mRNA is increased in high-inflammation schizophrenia midbrain. We hypothesised that increased mRNA expression for distinct NF-κB pathway members may be found, which could help identify specific triggers of midbrain inflammation. Midbrain tissue RNA extracted from age-matched schizophrenia patients (n = 62) and non-psychiatric controls (n = 62) was analysed using high-throughput qPCR for 15 major NF-κB related transcripts: six activating receptors (IL-1 receptor 1 [IL1R1], toll-like receptor 4 [TLR4], TNF receptor 1 [TNFR1], cluster of differentiation 40 [CD40], lymphotoxin β receptor [LTβR], TNFR2), three inducing kinases (inhibitor of nuclear factor κ-B kinase subunit β [IKKβ], IKKα, NF-κB-inducing kinase [NIK]), three NF-κB subunits (1 [NF-κB1], 2 [NF-κB2], v-rel avian reticuloendotheliosis viral oncogene homolog A [RelA]), and three inhibitors (human immunodeficiency virus type I enhancer binding protein 2 [HIVEP2], NF-κB inhibitor α [IκBα], IκBβ). We found significantly increased mRNA levels for four activating receptors (CD40, IL1R1, TNFR1, TNFR2), one inducing kinase (NIK), all three NF-κB subunits (NF-κB1, NF-κB2, RelA), and one inhibitor (IκBα) in schizophrenia. When stratified by inflammation status based on cytokine transcript levels, all of these nine transcripts were significantly elevated in the high-inflammation schizophrenia group, as was LTβR. Only IL1R1 mRNA was elevated in the low-inflammation schizophrenia group compared to low-inflammation controls. To explore which cells may be responsible for increased NF-κB pathway activation in schizophrenia, we conducted snRNA-seq on midbrain tissue from a subgroup of the same cohort (14 controls, 20 schizophrenia). NF-κB-related mRNA levels from both the canonical and the non-canonical pathway were highest in seven cell clusters (astrocytes, microglia, macrophages, endothelial cells, oligodendrocytes, T cells, and neurons). Endothelial cells were the only cells with substantial IL1R1, NF-κB2, and IκBα expression, whereas TNFR1 was mostly found in astrocytes, microglia, macrophages, and T cells. Together, these findings support that increased NF-κB induces cytokine mRNA expression in schizophrenia midbrain via multiple upstream activators and cell types. The widespread increase in multiple NF-κB transcripts highlights both redundant activation mechanisms and a putative attempt to control NF-κB activation. - Source: PubMed
Publication date: 2026/03/25
Neuhaus LaylaZhu YuntingClearwater Misaki SMendez-Victoriano GerardoWebster Maree JNewell Kelly AWalpole Samara JVieyra Rose ChesworthKarl TimWalker Adam KWeickert Cynthia S - BACKGROUND: Autosomal dominant intellectual developmental disorder type 43 (MRD43) is a rare neurodevelopmental disorder caused by mutations in the HIVEP2 gene. Although previous cases have established core phenotypic features, detailed descriptions of neuroimaging evolution and effective epilepsy management strategies remain limited. This case presents novel findings: it identifies a previously unreported pathogenic variant, documents dynamic changes in the corpus callosum, and details a successful combination antiepileptic drug regimen, providing comprehensive insights into the natural course and clinical management of this disorder. CASE PRESENTATION: We report a 14-year-old male who presented with global developmental delay, intellectual disability, and epilepsy. An initial brain magnetic resonance imaging (MRI) suggested slight thinning of the corpus callosum (involving the genu, rostrum, and body), though a subsequent review found no abnormalities. Genetic testing identified a novel de novo pathogenic variant in the HIVEP2 gene (NM_006734.4: c.3412 C > T, p.Q1138X), confirming the diagnosis of MRD43. His seizures were effectively controlled with a combination of levetiracetam and lamotrigine, which was accompanied by improvement in his electroencephalogram findings. CONCLUSIONS: This case expands the clinical and radiological spectrum of MRD43. The observation of evolving corpus callosum abnormalities suggests a previously underappreciated progressive neurodevelopmental component to the disorder. Furthermore, the positive response to combination antiepileptic therapy offers a practical management reference for clinicians. This report underscores the importance of longitudinal neuroimaging and tailored treatment in managing HIVEP2-related disorders. - Source: PubMed
Publication date: 2026/03/10
Zhu ZetongMa MingshuangCui XiaoyuShu JianboLiu Yang - β-Cell replacement therapy offers a potential cure for type 1 diabetes, but its success is limited by rapid graft rejection. While genome-wide CRISPR screens have recently identified RNLS and HIVEP2 as candidate genes capable of protecting β-cells from autoimmune destruction, their efficacy against the distinct mechanisms of allogeneic and xenogeneic rejection remains unknown. This study aimed to test the hypothesis that single-gene ablation of RNLS or HIVEP2 protects β-cell spheroids from allo- and xenorejection in immunocompetent hosts. - Source: PubMed
Publication date: 2026/02/03
Karaoglu Ismail CanOdabas ArdaÖnder TamerKizilel Seda - Methionine aminopeptidase 2 (METAP2), one of the two enzymes responsible for removing the N-terminal methionine from nascent proteins, has emerged as a potential drug target for cancer therapy. Yet, its role in ovarian cancer remains largely elusive. Here, we demonstrated that METAP2 is upregulated in ovarian cancer tissues and is associated with poor clinical outcomes. Consistently, METAP2 knockdown significantly suppresses the proliferation and migration of ovarian cancer cells in vivo and in vitro. Mechanistically, co-immunoprecipitation analysis identified YTHDF2 as a key interactor of METAP2. METAP2 interacts with YTHDF2 and attenuates its K48-linked ubiquitination at lysine 245, thereby preventing proteasomal degradation. Importantly, using AlphaFold3 algorithm, we elucidated and then experimentally validated that the Gln342 to Phe361 region of YTHDF2 interacts with the Thr240 to Gly358 region of METAP2. Furthermore, we identified BMF, LXRA, and HIVEP2 as functionally critical downstream targets of the METAP2-YTHDF2 axis, which are essential for ovarian cancer cells proliferation, migration and invasion. Additionally, we validated the therapeutic potential of the METAP2 inhibitor ZGN-1061 in ovarian cancer models. In conclusion, our findings reveal that METAP2 drives ovarian cancer progression by promoting YTHDF2-mediated mRNA decay of BMF/LXRA/HIVEP2, highlighting METAP2 as a potential therapeutic target for ovarian cancer. - Source: PubMed
Publication date: 2025/10/16
Wu LinxiangWu ChulingHe ShashaChen YuyingZhang YangXu HuishanLing QinZhang ZuweiSun TingtingYao ShuzhongRen YufengLai HuilingYang Guofen - Diminished ovarian reserve (DOR) is one of the most important reasons for decreasing fertility. Quercetin, a phytochemical, widely exists in food and natural Chinese herbs and can increase female fertility. However, how the phytochemical improves fertility through increasing ovarian reserve remains unclear. - Source: PubMed
Publication date: 2025/10/13
Xiao XianZheng MianZhao YingHuang KailiShi YuqingRen YiboChen LinlinSun JiaYe RanZheng ZihuiRuan Qinli