CAMK2B Antibody (C_term D406) Blocking Peptide
- Known as:
- CAMK2B Antibody (C_term D406) Blocking Peptide
- Catalog number:
- BP7417b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CAMK2B Antibody (C_term D406) Blocking Peptide
Related genes to: CAMK2B Antibody (C_term D406) Blocking Peptide
- Gene:
- CAMK2B NIH gene
- Name:
- calcium/calmodulin dependent protein kinase II beta
- Previous symbol:
- CAMKB
- Synonyms:
- CAM2, CAMK2
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-24
- Date modifiied:
- 2016-10-05
Related products to: CAMK2B Antibody (C_term D406) Blocking Peptide
Related articles to: CAMK2B Antibody (C_term D406) Blocking Peptide
- Colon cancer (CC) is a highly prevalent malignant tumor with a high mortality rate worldwide. Despite recent advancements in diagnosis and treatment, the overall prognosis for patients remains poor, especially for those with metastasis. Exploring key genes associated with the prognosis of patients with colon cancer, establishing effective molecular models, and validating their functions are necessary to optimize patient management and develop novel therapeutic strategies. This study aimed to reveal the role of the key gene SERPINE1 in the progression of colon cancer and its potential clinical application value through bioinformatics analysis and experimental validation. - Source: PubMed
Publication date: 2026/05/05
Li XinLi NanaWang YujieHan QixiangLi XiaodongTu QiushiSun BoshiYang HaoGao Yuan - Environmental neurotoxicants such as rotenone (RO) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) are known to induce cytotoxicity in neural cells. This study aimed to investigate the neuroprotective properties of active vitamin D3 against the cytotoxic effects of RO and MPTP on undifferentiated human neuroblastoma (SH-SY5Y) cells. Exposure to these neurotoxins resulted in concentration- and time-dependent reductions in cell viability. Cotreatment with vitamin D significantly mitigated the cytotoxic impact of both compounds. Furthermore, vitamin D attenuated disruptions in noradrenaline turnover and acetylcholinesterase activity caused by neurotoxin exposure. Mechanistic exploration revealed that vitamin D preserved cellular bioenergetics by maintaining ATP levels, supporting Mitochondrial Complexes I and III activities, stabilizing mitochondrial membrane potential and reducing lactate accumulation. Vitamin D also reduced oxidative stress, as evidenced by lower reactive species production and lipid peroxidation, while enhancing catalase (CAT) activity in treated cells. In addition, vitamin D counteracted the upregulation of neurodevelopmental genes CAMK2A and CAMK2B induced by neurotoxin exposure. Collectively, these findings demonstrate that vitamin D3 confers significant neuroprotection against RO- and MPTP-induced toxicity in SH-SY5Y cells by modulating mitochondrial function, oxidative stress and neurochemical balance. These results support the potential therapeutic use of vitamin D3 to prevent or ameliorate neurodegenerative conditions and other neurological disorders characterized by mitochondrial dysfunction and oxidative damage. - Source: PubMed
Elmorsy Ekramy MAl-Ghafari Ayat BAl Doghaither Huda AAly Nagwa MSalem Mai AToraih Eman AFawzy Manal SShehata Shaimaa A - Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis type 13 (ALS13) are triggered by polyglutamine expansion in Ataxin-2 (ATXN2). To understand these neurodegenerative disorders at the molecular level, the brains of 10-month-old -CAG100-knockin mice were analyzed as microglial, astroglial and neuronal fractions via global RNA sequencing. Data were validated by comparison with the spinal cord oligonucleotide microarray profile or filtered by RNA-seq consistency. Here, we show that the mutation causes a massive inflammatory response in microglia and a reciprocal loss of neuronal transcripts in glial fractions, suggesting severe synapse loss. Beyond these general neurodegenerative signs, we identify pathognomonic changes in the machinery for protein translation and RNA splicing. Glial fractions showed upregulation of (to 2082%), , , , , , , , and as an unspecific neuroinflammatory signature, versus downregulation of axonal (to <19%), and synaptic , , , and mRNAs correlating with circuit disconnection. In all fractions, reductions in , , and were noted versus disease-specific inductions of ribosomal subunits, presumably mirroring the partial loss-of-function of ATXN2 as RNA translation modulator. Selective accumulations of embryonic factors and versus downregulation of adult specify the mutation impact on splicing and translation elongation. As a potential underpinning of toxic gain-of-function, the proteostasis transcript appeared increased in astroglial and microglial fractions. These transcriptome data suggest altered ribosomal and spliceosome machinery, with massive microgliosis versus mild astrogliosis, at the core of SCA2 and ALS13. - Source: PubMed
Publication date: 2026/04/15
Auburger GeorgKandi Arvind ReddyVutukuri RajkumarAlmaguer-Mederos Luis-EnriqueGispert SuzanaSen Nesli-EceKey Jana - Coagulation dysfunction is a common complication of hepatocellular carcinoma (HCC) and is reflected clinically by the international normalized ratio (INR), yet its serum molecular correlates remain poorly defined. We aimed to identify an INR-associated serum multi-omics signature in HCC and characterize the underlying molecular networks. - Source: PubMed
Publication date: 2026/04/19
Cai YuyingLyu LingnaMa JiayiWang XiaoruMa WenxiaYin JimingWang Shanshan - Pathogenic variants in the calcium/calmodulin-dependent protein kinase II B gene (CAMK2B) have been associated with neurodevelopmental disorders, including epilepsy, yet the mechanisms underlying cortical dysfunction remain largely unclear. Building on our previous clinical report of a patient carrying the CaMKIIβ P213L variant and our prior characterization of the corresponding mouse models, we investigated how P213L-associated CaMKIIβ insufficiency alters cortical network dynamics and susceptibility to pentylenetetrazol (PTZ)-induced seizures in vivo. - Source: PubMed
Publication date: 2026/04/15
Mutoh HirokiAoto KazushiFukuda AtsuoSaitsu Hirotomo