CaMK2b antibody
- Known as:
- CaMK2b (anti-)
- Catalog number:
- orb10224
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CaMK2b antibody
Related genes to: CaMK2b antibody
- 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
Related articles to: CaMK2b antibody
- Liver fibrosis is a major global health burden with limited treatments. Emerging evidence suggests that metabolic dysregulation can create a state that makes the liver more prone to fibrosis. Carnitine, synthesized by γ-butyrobetaine hydroxylase (BBOX1), is crucial for fat metabolism, but the role of the BBOX1-carnitine axis in liver fibrosis is unclear. This study aimed to elucidate the functional impact of BBOX1 deficiency on hepatic fibrogenesis and to delineate the underlying mechanistic pathway. - Source: PubMed
Zhan YulingWang YingWei TianlongHe YingyuanLu ShiyiShao QianqianMa ShashaZhang LiMei XiaoqiangGao Yu - Calcium calmodulin kinase II (CaMKII) signaling is activated by muscle use and drives gene expression that promotes slow oxidative muscle phenotype. Previously, we showed that the calpain 3 knockout (C3KO) mouse model of limb girdle muscular dystrophy R1 (LGMDR1) exhibits impaired slow-oxidative gene expression and these deficits were associated with reduced levels of the CaMKIIβ isoform and attenuated CaMKII signaling in C3KO muscles. To investigate the contribution of CaMKIIβ signaling to the calpain 3-deficient phenotype, we generated both loss-of-function (muscle-specific conditional knockout, Camk2b cKO) and gain-of-function (muscle-specific overexpression of a constitutively active CaMK2b) models. Camk2b cKO muscles exhibited myopathic features and weakness and their muscles failed to upregulate genes that promote oxidative metabolism and stress-responses following endurance exercise, similarly to C3KO muscles. Mitochondrial respiration showed reduced activity of complex I, complex II and fatty acid oxidation. RNA sequencing of LGMDR1 patient biopsies revealed a similar reduction in genes involved in oxidative metabolism, aligning human and mouse findings. Overexpression of a constitutively active Camk2b in C3KO muscles enhanced oxidative metabolism and improved functional performance. Our results support the hypothesis that blunted CaMKIIβ signaling contributes to the failed upregulation of genes involved in oxidative metabolism and stress-responses in C3KO muscles. These studies highlight metabolic insufficiency as a central contributor to LGMDR1 pathogenesis and support the therapeutic potential of targeting CaMKII signaling to ameliorate disease features in LGMDR1. - Source: PubMed
Kramerova IrinaAnastopulos FriedaBecerra DianaGoldstein de Salazar RubyKeeble Alexander RChamberlain Jeffrey SMoore Steven AMcNally Elizabeth MSpencer Melissa J - 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