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anti-Human FGF13 Antibodies:
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The present study reported the presence of FGF13 in the follicular fluid of women undergoing IVF/ICSI. Moreover, the relationships between FF-FGF13 and FF-TT, ovarian morphology and oocyte developmental competence imply that FF-FGF13 might be involved in the pathophysiological process of polycystic ovary syndrome.
Autism-related protein MeCP2 regulates FGF13 expression and emotional behaviors
FGF13 was downregulated in human placentae with early-onset preeclampsia. FGF13 played an important role in maintaining placental trophoblast permeability via the modulation of E-cadherin.
We propose that, in cells in which activated oncogenes drive excessive protein synthesis, FGF13 may favor survival by maintaining translation rates at a level compatible with the protein quality-control capacity of the cell. Thus, FGF13 may serve as an enabler, allowing cancer cells to evade proteostasis stress triggered by oncogene activation.
Study screened the coding and splice site regions of the FGF13 gene in a sample of 45 unrelated probands where genetic epilepsy with febrile seizures plus segregated in an X-linked pattern; subsequently identified a de novo FGF13 missense variant in an additional patient with febrile seizures and facial edema. Results suggest that FGF13 is not a common cause of genetic epilepsy with febrile seizures plus.
identified two novel native phosphorylation sites in the C terminus of NaV1.5 that impair FGF13-dependent regulation of channel inactivation and may contribute to CaMKIIdeltac-dependent arrhythmogenic disorders in failing hearts.
These data showed the diversity of the roles of the FGF13 N-termini in NaV1.5 channel modulation and suggested the importance of isoform-specific regulation
the FGF13/Nav1.7 complex is essential for sustaining the transmission of noxious heat signals
for PCa patients after RP, FGF13 serves as a potential novel prognostic marker that improves prediction of BCR-free survival, in particular if combined with other clinical parameters.
The findings of this study reveal a novel cause of this syndrome and underscore the powerful role of FGF13 in control of neuronal excitability.
X-chromosome deletions may be a cause of WS with larger deletions being lethal to males and that FGF13 mutations may be a cause of Wildervanck Syndrome (WS).
Upregulated expression of FGF13/FHF2 mediates resistance to platinum drugs in cervical cancer cells
FGF13 has a role in hair follicle growth and in the hair cycle as shown in a family with X-linked congenital generalized hypertrichosis
interactions with perlecans
identification of a domain controlling angiogenic properties
FHF2B is an interacting partner of Na(v)1.6. The preferential expression of FHF2B in sensory neurons may provide a basis for physiological differences in sodium currents that have been reported at the nodes of Ranvier in sensory versus motor axons.
FHF2 has an essential role in dictating myocardial excitability and conduction that safeguards against temperature-sensitive conduction failure
regulator of caveolae-mediated mechanoprotection and adaptive hypertrophic signaling in cardiomyocytes
These results implicate that FGF13 is a critical cardiac Na(+) channel modulator and Fgf13 knockout mice have increased arrhythmia susceptibility in the setting of Na(+) channel blockade.
FGF13 down-regulated Spry1 protein expression, activating the ERK1/2 pathway by phosphorylation and leading to C2C12 cell differentiation inhibition.
Fibroblast growth factor homologous factors (FGF11-14) modulate cardiac calcium channels.
FGF13 has a role in hair follicle growth and in the hair cycle
Genetic deletion of FGF13 in mice results in neuronal migration defects in both the neocortex and the hippocampus. FGF13-deficient mice also exhibit weakened learning and memory.
Fibroblast growth factor homologous factor 13 regulates Na(V)1.5 sodium channels and conduction velocity in murine hearts.
FGF-13 may play a role in regulating the function of cells in the bulge region and basal layer of the epidermis.
The protein encoded by this gene is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth, and invasion. This gene is located in a region on chromosome X, which is associated with Borjeson-Forssman-Lehmann syndrome (BFLS), making it a possible candidate gene for familial cases of the BFLS, and for other syndromal and nonspecific forms of X-linked mental retardation mapping to this region. Alternative splicing of this gene at the 5' end results in several transcript variants encoding different isoforms with different N-termini.
, fibroblast growth factor 13
, Fibroblast growth factor 13
, fibroblast growth factor homologous factor 2