Human Calcitonin gene-related peptide 2 CALCB
- Known as:
- Human Calcitonin gene-related short protein sequence 2 CALCB
- Catalog number:
- CH09
- Product Quantity:
- l0
- Category:
- -
- Supplier:
- Novoprotein
- Gene target:
- Human Calcitonin gene-related peptide 2 CALCB
Related genes to: Human Calcitonin gene-related peptide 2 CALCB
- Gene:
- CALCB NIH gene
- Name:
- calcitonin related polypeptide beta
- Previous symbol:
- CALC2
- Synonyms:
- FLJ30166, CGRP-II
- Chromosome:
- 11p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-02-22
Related products to: Human Calcitonin gene-related peptide 2 CALCB
Related articles to: Human Calcitonin gene-related peptide 2 CALCB
- Genetic aberrations are among the critical driving factors of lung cancer. Importantly, the impact of genetic variations on proteomic dysregulations with the goal of characterizing potential diagnostic biomarkers at the population-level requires additional investigation. Modeling such proteogenomic interactions is crucial in understanding early-stage biological disruptions to inform biomarker discovery, successful clinical trials, and developing effective therapeutics. - Source: PubMed
Publication date: 2026/03/13
Johnson Marcela ANieves-Rodriguez ShirleyHou LipingHuang Bevan EmmaSaadatpour AssiehDoostparast Torshizi Abolfazl - The microtubule-stabilizing drug paclitaxel remains the standard of care for various solid malignancies but frequently leads to chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a leading cause for premature treatment termination and a significantly reduced quality of life in long-term cancer survivors. The molecular mechanisms of neuro-axonal degeneration, neuroinflammation, and pain in patients treated with paclitaxel remain incompletely understood, and there are currently no predictive biomarkers or preventive treatments. We used human iPSC-derived sensory neurons exposed to paclitaxel to comprehensively model the pathophysiology of CIPN. Neurotoxicity was assessed over time using viability assays and sequential RNA sequencing, as well as deep proteome and lipidomic analyses. We observed a time and dose-dependent decline of cell viability at clinically relevant paclitaxel doses. Sequential RNA sequencing defined JUN as an early immediate gene, followed by the overexpression of genes of the neuronal stress response (e.g., ARID5A, WEE1, DUSP16, GADD45A), neuronal injury and apoptotic pathways (e.g., ATF3, HRK, BBC3 [PUMA], BCL2L11 [BIM], CASP3), neuroinflammation and nociception (CALCB, MMP10, IL31RA, CYSLTR2, C3AR1, TNFRSF12A) and neuronal transduction (e.g., CAMK2A, STOML3, PIRT), while key enzymes of lipid biosynthesis were markedly downregulated (e.g., LSS, HMGCS1, HMGCR, DHCR24). Deep proteome analyses following 48 h of exposure to 100 nM paclitaxel revealed a strong correlation of differentially expressed RNA with proteins, and a marked degradation of essential axonal transport proteins such as kinesins, stathmins, and scaffold proteins. Consistent with the downregulation of rate-limiting enzymes of lipid biosynthesis, lipidome analysis confirmed deregulation of neuronal lipid homeostasis. In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets. - Source: PubMed
Publication date: 2026/02/10
Schinke ChristianMaierhof Smilla KHew LoisFernandez Vallone ValeriaFrahm SilkeTelugu Narasimha SwamyDiecke SebastianIvanov AndranikKovács RichardBeule DieterKirchner MarieluiseMertins PhilippBrüning UlrikeKirwan Jennifer AStachelscheid HaraldEndres MatthiasHuehnchen PetraBoehmerle Wolfgang - Procalcitonin (PCT) is a biomarker used to differentiate between viral and bacterial infections, though the underlying mechanisms are not yet fully understood. This study aimed to identify genetic variants associated with plasma PCT concentrations and explore the associations of genetically predicted PCT with a wide range of disease related traits in a PheWAS. - Source: PubMed
Publication date: 2025/12/16
Zhang Wenbovan der Most Peter JWang SiqiKamali ZohaGiontella AliceEnhörning SofiaGansevoort Ron Tvan der Harst PimBakker Stephan J LMelander OlleKeus FrederikLunter GertonSnieder Harold - Migraine is a common chronic condition with a clear need for innovative treatment approaches. Protein quantity trait loci (pQTLs), which specifically regulate protein expression levels, are the closest and most stable QTLs to the phenotypes under study. In this context, we employ plasma proteomes data to conduct Mendelian randomization and colocalization analysis to identify potential drug targets for migraine. Plasma proteome data were sourced from the Decode, UKB-PPP, and Interval databases. We selected cis-SNPs associated with plasma protein levels at a genome-wide significance level (p < 5 × 10) as instrumental variables for Mendelian randomization analysis. Using the IEU OpenGWAS database (NCase = 13,971, NControl = 470,627) as an outcome, we initially explored the causal relationship with migraine through summary-data-based Mendelian randomization (SMR). We conducted a multi-tiered screening, including two-sample MR, HEIDI test, and Bayesian colocalization to confirm potential targets related to migraine. Additionally, we included GWAS data from the UK Biobank (NCase = 13,597, NControl = 449,336) for further robustness validation. Our initial SMR analysis identified 11 plasma proteins with potential causal links to migraine. Further investigation through two-sample Mendelian randomization using inverse variance weighted analysis (IVW) and sensitivity analysis yielded 8 significant proteins. These included 6 double-positive proteins (CALCB, COLEC11, SEMA6C, SERPING1, TBC1D17, UBE2L6) and 2 single-positive proteins (HYOU1, SERPINA1), all meeting criteria in the HEIDI test (P > 0.05) and colocalization analysis (PP.H > 0.7). External validation using an alternate migraine GWAS dataset (non-cancer illness code, self-reported: migraine ukb-b-16868) confirmed the findings for 5 proteins. Both HEIDI test and Bayesian colocalization suggested robust positive results for CALCB and TBC1D17. Specifically, CALCB is associated with an increased risk of migraine, whereas TBC1D17 is associated with a reduced risk. Our research provides strong evidence for two proteins and suggestive evidence for three additional proteins as potential targets for migraine treatment. Notably, CALCB is already under development as a therapeutic target for migraines, lending credibility to the promising drug development prospects for TBC1D17. Future studies are needed to confirm the causal role of TBC1D17 and explore the underlying mechanisms in migraine. - Source: PubMed
Publication date: 2025/11/25
Guo LongxinLi JianChen ZheZhang XinyueLi Chengxian - Peripheral neuropathy is a common complication in diabetes, affecting around 50% of the diabetic population. Co-occurrence of diabetic peripheral neuropathy (DPN) and diabetic bone disease has led to the hypothesis that DPN influences bone metabolism, although little experimental evidence has yet supported this premise. To investigate, mice were fed a high-fat diet (HFD) followed by phenotyping of skeletal-innervating neurons and bone architectural parameters. Results showed that HFD feeding resulted in a marked decrease in skeletal innervation (69%-41% reduction in Beta-III-Tubulin-stained nerves, 38% reduction in CGRP-stained nerves in long bone periosteum). These changes in skeletal innervation were associated with significant alterations in bone mass and in cortical and trabecular bone microarchitecture of long bones. Single-cell RNA sequencing (scRNA-Seq) of sensory neurons and bone tissue was next utilized to reconstruct potential nerve-to-bone signaling interactions, including implication of sensory nerve-derived neurotrophins (Bdnf), neuropeptides (Gal, Calca and Calcb), and other morphogens (Vegfa, Pdgfa, and Angpt2). Moreover, scRNA-Seq identified marked shifts in periosteal cell transcriptional changes within HFD-fed conditions, including a reduction in cell proliferation, an increase in adipogenic differentiation markers, and reductions in WNT, TGFβ, and MAPK signaling activity. When isolated, periosteal cells from HFD-fed mice showed deficits in proliferative and osteogenic differentiation potential. Moreover, these cellular changes in proliferation and differentiation capacity were restored by treatment of HFD-exposed periosteal cells to sensory neuron-conditioned medium. In summary, HFD modeling of type 2 diabetes results in skeletal polyneuropathy. Moreover, the combination of multi-tissue scRNA-Seq and isolated in vitro studies strengthen the case for altered nerve-to-bone signaling in diabetic bone disease. - Source: PubMed
Publication date: 2025/07/04
Cherief MasnsenGomez-Salazar MarioKang MinjungLee SeungyongRamesh SowmyaQin QizhiXu MingxinKim SoohyunArcher MaryZhu ManyuHoke AhmetJames Aaron W