Calcitonin Gene Related Peptide II, human Formula C162H267N51O48S3 Sequence Ala_Cys_Asn_Thr_Ala_Thr_Cys_Val_Thr_His_Arg_Leu_Ala_Gly_Leu_Leu_Ser_Arg_Ser_Gly_Gly_Met_Val_Lys_Ser_Asn_Phe_Val_Pro_Thr_As
- Known as:
- Calcitonin Gene Related Peptide II, H. sapiens Formula C162H267N51O48S3 Sequence Ala_Cys_Asn_Thr_Ala_Thr_Cys_Val_Thr_His_Arg_Leu_Ala_Gly_Leu_Leu_Ser_Arg_Ser_Gly_Gly_Met_Val_Lys_Ser_Asn_Phe_Val_Pro_Thr_As
- Catalog number:
- 52232
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- GLSChina
- Gene target:
- Calcitonin Gene Related Peptide human Formula C162H267N51O48S3 Sequence Ala_Cys_Asn_Thr_Ala_Thr_Cys_Val_Thr_His_Arg_Leu_Ala_Gly_Leu_Leu_Ser_Arg_Ser_Gly_Gly_Met_Val_Lys_Ser_Asn_Phe_Val_Pro_Thr_As
Related genes to: Calcitonin Gene Related Peptide II, human Formula C162H267N51O48S3 Sequence Ala_Cys_Asn_Thr_Ala_Thr_Cys_Val_Thr_His_Arg_Leu_Ala_Gly_Leu_Leu_Ser_Arg_Ser_Gly_Gly_Met_Val_Lys_Ser_Asn_Phe_Val_Pro_Thr_As
- Gene:
- FOXD3 NIH gene
- Name:
- forkhead box D3
- Previous symbol:
- -
- Synonyms:
- Genesis, HFH2
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: Calcitonin Gene Related Peptide II, human Formula C162H267N51O48S3 Sequence Ala_Cys_Asn_Thr_Ala_Thr_Cys_Val_Thr_His_Arg_Leu_Ala_Gly_Leu_Leu_Ser_Arg_Ser_Gly_Gly_Met_Val_Lys_Ser_Asn_Phe_Val_Pro_Thr_As
Paliperidone N-Oxide CAS: 761460-08-6 Formula: C23H27FN4O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3,16α-diol CAS: 90474-20-7 Formula: C20H24Br2O4 2,4-Dibromo-17,17-ethylenedioxy-1,3,5(10)-estratriene-3-ol CAS: Formula: C20H24Br2O3 3,3',5,5'-Tetraiodo Thyroformic Acid CAS: 2055-97-2 Formula: C13H6I4O4 3,5,3',5'-Tetrachlorobisphenol A CAS: 79-95-8 Formula: C15H12Cl4O2 4-(2,6,6-Trimethyl-2-cyclohexen-1-ylidene)-2-acetoxybut-2-ene CAS: 61693-39-8 Formula: C15H22O2 4-Benzyloxy-1-cyclohexanecarbonitrile (cis / trans mixture) CAS: 95233-32-2 Formula: C14H17NO 5-[(4-Methoxyphenyl)-diphenylmethylamino-6-methoxy-9H-purin-9-yl]-13C2, 15N-3-(phenylmethoxy)-2-[(phenylmethoxy)methyl]-cyclopentanol CAS: Formula: 6-Phenylhexylamine Hydrochloride CAS: 120375-57-7 Formula: C12H20ClN Paliperidone-d4 CAS: 1020719-55-4 Formula: C23H23D4FN4O3 [Tyr63] PTH (63_84), human
Human ELC ELISA KIT 96 TEST
"Recombinant Human Carboxypeptidase E_CPE""Recombinant Human Carboxypeptidase E_CPE""Recombinant Human Carboxypeptidase E_CPE" Related articles to: Calcitonin Gene Related Peptide II, human Formula C162H267N51O48S3 Sequence Ala_Cys_Asn_Thr_Ala_Thr_Cys_Val_Thr_His_Arg_Leu_Ala_Gly_Leu_Leu_Ser_Arg_Ser_Gly_Gly_Met_Val_Lys_Ser_Asn_Phe_Val_Pro_Thr_As
- Fetal alcohol spectrum disorders (FASD) exhibit wide phenotypic variability not explained by prenatal alcohol exposure (PAE) alone. While genetic factors may modify vulnerability, there are no prior FASD genome-wide association studies (GWAS). We performed genome-wide single-marker and gene-based analyses of two South African prospective birth cohorts (Cape Town Longitudinal Cohorts (CTLC); n=328 mother-child dyads) and the US Collaborative Initiative on Fetal Alcohol Spectrum Disorders cohort (CIFASD n=429 children only). We examined main genetic and gene-by-PAE interaction effects on working memory, recognition memory, height, and FASD diagnosis using single-marker and gene-based analyses and the Haplotype-based Transmission Disequilibrium Test (HTDT), which integrates maternal-child genetics. Genome-wide genotype array data were used; TOPMed-imputed data were used to refine results. Risk-modifying genes were then tested for differential mRNA expression based on PAE in placenta and child blood. Gene*PAE interaction gene-based analyses identified STX6 associated with height-for-age Z-scores (p=2.2×10⁻⁶) and FOXD3 with recognition memory performance (p=4.7×10⁻⁶) in children. Single-marker analysis detected one child SNP approaching significance (rs2833924, p=8.8x10-8) with Gene*PAE interaction for working memory performance. CTLC+CIFASD meta-analysis in children identified one significant locus (HTR1E; pmeta=2.75×10⁻⁶) with Gene*PAE interaction for working memory performance. The HTDT test in CTLC imputed data identified three haplotypes associated with FASD diagnosis risk: COP1 (padj=0.029), WWOX (padj=2×10⁻4), TMEM38B (padj= 0.019). WWOX, STX6, and TMEM38B were differentially expressed in placenta and/or child blood based on PAE. In this first-ever genome-wide investigation of maternal and child genetics in FASD, we identified multiple biologically plausible risk-modifying loci for FASD neurobehavioral, growth, and FASD diagnosis outcomes. - Source: PubMed
Publication date: 2026/09/10
Carter RobertRuhela VivekLesseur CorinaCilleros-Portet AriadnaJacobson Sandra WJacobson Joseph LMeintjes ErnestaDodge NeilAkkaya-Hocagil TugbaHoyme H EugeneCheng HaoxiangChen JiaHao KeDeyssenroth Maya ATosto Giuseppe - KRAS G12C mutation is a clinically relevant driver in non-small cell lung cancer (NSCLC), yet the signaling networks that modulate malignant behavior in this context remain incompletely defined. In this study, we examined the functional role of FOXD3 and its relationship with NF-κB signaling in KRAS G12C-mutant NSCLC models. Stable FOXD3 overexpression was established in SW1573 and LU65 cells. FOXD3 reduced cell viability, migration, and invasion while increasing caspase 3/7 activity in both cell lines. Transcriptomic profiling in LU65 cells followed by Hallmark enrichment analysis identified TNFα signaling via NF-κB as a prominently altered pathway associated with FOXD3 overexpression. Consistently, NF-κB dual-luciferase assays showed reduced basal NF-κB transcriptional activity in FOXD3-overexpressing cells. TNFα stimulation partially reversed the inhibitory effects of FOXD3 on proliferation, migration, and invasion and attenuated FOXD3-induced apoptosis. In addition, stable FOXD3 overexpression suppressed xenograft growth in vivo. Collectively, these findings support a functional association between FOXD3 overexpression and reduced NF-κB-related transcriptional activity in KRAS G12C-mutant NSCLC models, although the present data do not establish direct causal mediation by NF-κB. - Source: PubMed
Publication date: 2026/08/28
Xu PengzhenPeng JieGuo ChaoLiu ZhuCao YufengSheng QingXu WenfeiLi Xuhui - Diabetic cataract (DC) is a lens-opacity complication of diabetes driven by hyperglycemia-related oxidative, apoptotic, metabolic, and epithelial-mesenchymal transition (EMT) pathways. This review evaluated the expression and mechanistic roles of long non-coding RNAs (lncRNAs) and lncRNA-related epitranscriptomic regulators in DC. - Source: PubMed
Publication date: 2026/08/12
Chen Kai-YangChan Hoi-ChunChan Chi-Ming - Body color brightness is a key determinant of ornamental value in koi, yet nutritional strategies targeting structural coloration mediated by iridophores remain underexplored. Fish scale meal (FSM), an abundant fishery by-product, contains guanine and collagen, which may contribute to structural coloration and body brightness. This study evaluated the effects of partial replacement of fish meal with FSM on growth performance, body color parameters, pigment accumulation, iridophore density, and iridophore-related gene expression in koi. A total of 384 koi with an initial body weight of 19.02 ± 0.18 g were randomly assigned to six dietary treatments for 8 weeks, with FSM inclusion levels ranging from 0% to 9.55%, corresponding to 0-100% replacement of dietary fish meal. Growth performance, including final body weight, weight gain rate, and specific growth rate, decreased with increasing FSM inclusion. Body lightness (L*) and scale guanine content increased progressively with FSM level and reached their highest values at 9.55% FSM, whereas redness (a*), yellowness (b*), and total carotenoid content showed the opposite trend. Iridophore density was significantly higher in the 3.82-5.73% FSM groups than in the other treatments. The expression of iridophore-related genes, including , , , , and , showed non-linear responses and generally reached higher levels at moderate FSM inclusion, whereas showed an opposite transcript pattern. Overall, dietary FSM inclusion elicited trait-dependent responses in koi. Low or no FSM inclusion was preferable for maintaining growth, intermediate inclusion was more favorable for iridophore development, whereas higher FSM inclusion enhanced brightness-related traits. These findings suggest that FSM should be used according to the intended production objective, with inclusion levels adjusted for growth maintenance, iridophore-related coloration improvement, or brightness enhancement. - Source: PubMed
Publication date: 2026/07/19
Gao ShengyuXu XiaolongDing TongCheng YunxinZhang JiayueZheng HuiyiZhou ZuoqinLiu EnXu GaoxiaoHe Chaofan - The unique nature of neural crest cells has encouraged the characterization of the dorsal neural tube as distinct from the rest of the neural tube. Yet the dorsal and ventral neural tube have several similarities during neurulation, both acting as hinge points and opposing signaling centers. Furthermore, we find that the neural crest marker gene FOXD3, is expressed in both the dorsal and ventral neural tube, indicating shared roles unrelated to neural crest specification. This project aimed to identify genes coexpressed in the dorsal and ventral neural tube and characterize ventral FOXD3 function. - Source: PubMed
Publication date: 2026/07/06
Rees JenaidTaroc Ed ZandroBarbosa-Sabanero KarlaKirkland JamiyaMehedincu StefaniaSchiffmacher AndrewKerosuo Laura