Ask about this productRelated genes to: FGF13 antibody
- Gene:
- FGF13 NIH gene
- Name:
- fibroblast growth factor 13
- Previous symbol:
- -
- Synonyms:
- FHF2, FGF2
- Chromosome:
- Xq26.3-q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-16
- Date modifiied:
- 2018-02-13
Related products to: FGF13 antibody
Related articles to: FGF13 antibody
- Multiple myeloma (MM) is a malignant plasma cell disease inducing osteolytic lesions by disrupting bone homeostasis, fostering catabolic and suppressing anabolic functions. While the impact on osteoblast generation and function is well documented, alterations of osteocyte function and extracellular matrix (ECM) are not yet fully understood. Thus, using a syngeneic mouse model of MM by injecting MOPC315.BM cells intratibially into BALB/c mice (n = 95), we performed transcriptomic profiling of an osteocyte-enriched population and identified a mechanosensitive matrisomal gene signature, which was disrupted by tumor engraftment. Non-invasive tibial loading restored the expression of 94 ECM-associated genes, including collagens, fibronectin, and aggrecan. Cross-species integration with RNA-sequencing data from 387 MM patients revealed eight ECM-related genes whose expression correlated with overall survival (VEGFA, BCAN, FGF13, TNFSF8, SDC1, LAMC1, SEMA3A, and CCL2). Four of these genes (Vegfa, Sdc1, Sema3a, Ccl2) were also load-responsive in a murine osteocyte (IDG-SW3 cells) bioreactor model. Our findings indicate that an existing mechanosensitive osteocytic repair program is suppressed by MM cells, which can be reinvigorated via a brief single loading session. It suggests that exercise-based interventions may be beneficial to restore bone mass through endochondral ossification programs in patients with MM. - Source: PubMed
Publication date: 2026/09/07
Ziouti FaniAzeem MuhammadRummler MaximilianRosolowski MaciejZapata GerardoRindt WyonnaJulien CatherineTauer Josephine TCheng Wen-HuiBeck SusanneSeckinger AnjaHose DirkLeich EllenBogen BjarneLynch Maureen EKuric MartinKrug MelanieEbert ReginaZaucke FrankJakob FranzWillie Bettina MJundt Franziska - To explore the pathogenicity and prenatal counseling strategies for five Chinese pedigrees harboring a hemizygous c.-32C>G (NM_001139500.2) variant of fibroblast growth factor 13 (FGF13) gene. - Source: PubMed
Huang JiaWang JingyuanZhou LinxiaoYang HengYang WenjieChen ShuaiLiu Hongyan - Indigenous chickens in Eritrea are raised mainly in low-input village systems and show marked variation in body size, including reduced body size phenotype, a trait associated with reduced feed consumption, thermotolerance, disease resistance, and adaptability to resource-limited environments. This study aimed to identify genomic regions associated with reduced body size using a genome-wide association study (GWAS) in Eritrean chicken ecotypes. Blood samples from 384 ICs across 16 ecotypes (21 to 24 birds per ecotype) were genotyped using DArTseq technology. Three putative short-bodied ecotypes, Barentu (BAR), Foro (FORO), and Gogne (GOG), were compared with five heavier control ecotypes: Fshe-Mrara (FM), Adi-Tekeliezan (ADTEK), Emni-Haili (HAYL), Dekemhare (DEKE), and Adikeyh (KEIH). After filtering for individual missingness, marker call rate, and minor allele frequency, 141 birds and 42,356 SNP remained. Population structure was evaluated by principal component analysis and ADMIXTURE. Exploratory case-control GWAS were conducted for each putative reduced-body-size ecotype and for the 3 ecotypes combined. Complementary quantitative-trait GWAS used body weight, body length, back length, and shank length was carried out. Linear mixed models implemented in GEMMA included sex as a fixed effect and genomic kinship as a random effect. The first 2 principal components showed extensive ancestry sharing, although GOG was more differentiated. Ecotype-specific analyses identified significant regions near CDK6, BDNF, FOXP1, TNS3, and LGR4 in FORO; EIF2AK2, NANP, MDH1, UGP2 and FGF13 in GOG; and HMGA2, IGF2, BRSK1 and SUCNR1 in BAR. The combined analysis showed no genome-wide significant variants but revealed suggestive signals near ASAP1, EIF2AK2, and FOXP1, indicating a polygenic and ecotype-specific architecture. Overlapping candidate genes across analyses included TH (common to all) and EIF2AK2 (present in all ecotypes except FORO). Quantitative-trait analyses detected a single significant SNP within CACNB4 for back length, but none for the other traits. Overall, reduced body size in Eritrean IC appears to be a complex trait controlled by multiple loci, involving both conserved growth regulators and genes related to metabolic efficiency and environmental adaptation. These findings provide a genomic basis for future breeding strategies to improve productivity, resilience and sustainability of village poultry production systems in resource-limited regions of Eritrea. - Source: PubMed
Publication date: 2026/07/27
Habteslasie Hortuma APerini FrancescoNgeno KiplangatColombi DanieleLasagna EmilianoDessie TadelleKahi Alexander - The aim of this study was to detect genomic regions and genes associated with gastrointestinal nematodes (GIN) resistance in Pelibuey sheep, based in deworming necessity (NOD) estimated by fecal egg count (FEC). During a ten-months period, deworming criterion was based on GIN eggs per gram (EPG), then animals exceeding 1000 EPG were dewormed, and individuals were classified as cases (dewormed at least once) or controls (non-deworming at all). Animals were genotyped with the GGP Ovine50k genome profiler microarray. Quality control of dataset and case-control GWAS were carried to identify associated candidate genes and quantitative trait loci (QTL). Two genome-wide strongly associated SNPs were detected on chromosomes 2 and 3, located near FEC associated QTLs and immune-related genes: GALNT6, KLRK1, KLRD1, CLEC1B, FGF13, TMEM52B, OLR1, and CLEC7A. The identified genes are involved in key defense mechanisms such as mucus synthesis, immune signaling, and natural-killer cell activation, supporting their relevance as candidate genes for GIN-resistance selection in Pelibuey hair-sheep. - Source: PubMed
Publication date: 2026/07/04
Esparza-Acebo Leilany MargaritaOjeda-Robertos Nadia FlorenciaDe La Rosa-Reyna Xochitl FabiolaParra-Bracamonte Gaspar Manuel - Voltage-gated sodium (Nav) channels are key determinants of neuronal excitability, shaping action potential waveforms, repetitive firing patterns and responses to synaptic inputs, as well as controlling the output of neural circuits and influencing short- and long-term plasticity and homoeostasis. The firing and response properties of mammalian central neurons are highly variable, reflecting differences in the Nav (and other) channels expressed and the synaptic connectivity of the circuits in which the cells participate. Transient (I), persistent (I) and resurgent (I) Nav current components have been distinguished, and considerable progress has been made in defining their roles in regulating the firing properties of central neurons and the mechanisms underlying their generation. In addition, it is well established that native neuronal Nav channels function in macromolecular complexes, comprising a pore-forming α subunit assembled with multiple accessory/auxiliary proteins that influence channel expression, localization and biophysical properties. In mature central neurons, the Nav1.1, Nav1.2 and Nav1.6 α subunits are differentially expressed, together with one or more of the Nav beta (Navβ1-4), intracellular fibroblast growth factor (iFGF11-14), ankyrin (Ankyrin-B, -G, -R) and other auxiliary proteins, generating Nav channels with diverse cell-type- and circuit-specific expression patterns, subcellular distributions, gating properties, and physiological roles. Variants in the genes encoding these Nav α subunits (SCN1A, SCN2A, SCN8A), as well as Navβ1 (SCN1B), iFGFs (FGF12, FGF13, FGF14), ankyrins (ANK1, ANK2, ANK3), and other Nav channel auxiliary and interacting proteins, have been linked to several congenital neurological disorders, including epilepsy and ataxia, as well as to neurodevelopmental, neurodegenerative and psychiatric diseases. - Source: PubMed
Publication date: 2026/08/05
Ransdell Joseph LNerbonne Jeanne M