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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 (show RAB1A Antibodies) 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 (show SCN5A Antibodies) 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 (show SCN5A Antibodies) channel modulation and suggested the importance of isoform-specific regulation
the FGF13/Nav1.7 (show SCN9A Antibodies) complex is essential for sustaining the transmission of noxious heat signals
for PCa (show FLVCR1 Antibodies) patients after RP, FGF13 serves as a potential novel prognostic marker that improves prediction of BCR (show BCR Antibodies)-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
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 (show FGF11 Antibodies)-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.
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