CaMK2b antibody (FITC)
- Known as:
- CaMK2b (anti-) (fluorecein)
- Catalog number:
- orb15220
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CaMK2b antibody (FITC)
Related genes to: CaMK2b antibody (FITC)
- 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 (FITC)
Related articles to: CaMK2b antibody (FITC)
- Recent studies have found that the reticulophagy pathway is able to clear excess endoplasmic reticulum to protect cells from endoplasmic reticulum stress-induced damage. The role of reticulophagy in prostate cancer is still unknown. Key genes of reticulophagy were studied. Subsequently, the ULK3 and CAMK2B mRNA levels were confirmed. ULK3 and CAMK2B expression were elevated in prostate cancer tissues. The silencing of ULK3 inhibited prostate cancer cell vitality. The overexpression of ULK3 had the opposite effect. ULK3 was able to enhance the CAMK2B protein expression by promoting the entry of GLI1 into the nucleus, thereby upregulating the level of reticulophagy. Knockdown of CAMK2B could inhibit reticulophagy induced by ULK3. Further experiments showed that ULK3 phosphorylated GLI1, promoted its nuclear entry and binding to the CAMK2B promoter to enhance CAMK2B expression. Down-regulation of ULK3 inhibited the growth of prostate cancer vitality in vivo. This study confirmed that ULK3 promoted the prostate cancer by upregulating GLI1/CAMK2B-induced reticulophagy. - Source: PubMed
Publication date: 2026/06/15
Wang Qin-QuanSun ChenWu Jin-HuaYu Dong-DongZhou Hui-Liang - Olanzapine (OLZ), a commonly prescribed atypical antipsychotic, is strongly linked to cardiometabolic disorders (CMDs) such as obesity, insulin resistance, dyslipidemia, and cardiac dysfunction. Garcinia indica Choisy (kokum), a nutrient-rich medicinal fruit with antioxidant, anti-obesity, antidiabetic, and cardioprotective properties, has not yet been investigated for its potential to counter OLZ-induced CMD(s). This study examined the protective effects and underlying mechanisms of G. indica hydroalcoholic extract (GIE) against OLZ-induced cardiometabolic alterations using in vitro and computational approaches. GIE significantly reduced OLZ-induced cytotoxicity in H9c2(2-1) cardiomyocytes by lowering lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and nitric oxide (NO) levels, while enhancing glucose utilization. Gene expression analysis showed downregulation of IL6, BAX, CASP3, and CAMK2B, alongside upregulation of BCL2, indicating anti-inflammatory and anti-apoptotic modulation. Network pharmacology and in silico analyses identified thirteen phytocompounds targeting 35 CMD-related proteins, with gambogic acid- RAGE and amentoflavone- CALM1 interactions demonstrating the strongest binding affinities, supported by docking and molecular dynamics simulations. Overall, GIE exhibits multi-target regulatory effects on oxidative, inflammatory, and metabolic pathways, suggesting its therapeutic potential in mitigating OLZ-induced cardiometabolic disturbances. The current findings indicate promising mechanistic potential of GIE against OLZ- induced cardiometabolic alterations, warranting further validation through in vivo and clinical studies. - Source: PubMed
Beerwala Faizan AKolambkar Shruti VKarikazi AdilmehadiPatil Vishal SCharla RajithaGujarathi Swarup SBhandare Vishwambhar VDarasaguppe Harish RKhatib Nayeem ARoy Subarna - 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