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TMPRSS3 contributed to gastric cancer progression via activation of the PI3K/Akt/ERK signaling pathway.
Pathogenic variants in the TMPRSS3 gene in a cohort of 2247 subjects with sensorineural hearing loss represented 13 different rare TMPRSS3 variants, nine of which were novel.
knockdown of TMPRSS3 inhibits proliferation, migration, and invasion in human nasopharyngeal carcinoma cells through the inactivation of the PI3K/Akt signaling pathway. This study suggests that TMPRSS3 may be a potential therapeutic target for the treatment of nasopharyngeal carcinoma
For those with a combination of severely pathogenic TMPRSS3 variants, rapid aggravation of the residual hearing should be anticipated and treated accordingly. Our confirmation of the genotype-phenotype correlation of the TMPRSS3 gene may pave the way for the establishment of a personalized auditory rehabilitation.
Our results indicate that mutations in TMPRSS3 account for about 4.6% (7/151) of Chinese autosomal recessive nonsyndromic hearing loss cases lacking mutations in SLC26A4 or GJB2 and that the recurrent TMPRSS3 mutation p.Ala306Thr is likely to be a founder mutation.
Given that a previous paper suggested TMPRSS3 and GJB2 genes as responsible for a digenic form of hearing loss, our data support and reinforce this hypothesis.
In conclusion, TMPRSS3 and TNFRSF11B may have potential prognostic value to be used as tumor biomarkers in breast cancer patients.
different combinations of TMPRSS3 mutations led to different hearing impairment phenotypes (DFNB8/DFNB10) in the Chinese family.
TMPRSS3 mutations seem to be an important cause of autosomal recessive nonsyndromic hearing loss in Slovenia resulting in rather uniform phenotype with profound congenital hearing loss.
Study demonstrated that TMPRSS3 contributes to ovarian cancer cell proliferation, invasion and metastasis, probably via activation of the ERK1/2 signaling pathway.
TMPRSS3 expression is an independent prognostic factor for breast cancer patients. Bioinformatic analysis of potential TMPRSS3 binding proteins revealed that TMPRSS3 could be a key regulator of cancer pathways.
Low expression levels of hepsin and TMPRSS3 are associated with poor breast cancer survival
Single nucleotide polymorphisms in TMPRSS3 (rs3814903 and rs11203200) are significantly associated with breast cancer risk.
homozygous mutation TMPRSS3: c.535G>A causes prelingual hearing loss in this Tibetan family
The prevalence of TMPRSS3 mutations among Korean postlingual hearing loss is 8.3 %. The p.A306T variant of TMPRSS3 is the common founder allele in Koreans. A novel variant, p.T248M of TMPRSS3, was predicted to have milder pathogenicity.
Description of the spectrum of mutations in TMPRSS3 in 374 families with autosomal recessive, non-syndromic hearing loss from India.
Association between TMPRSS3 genotypes and phenotype variants in autosomal recessive nonsyndromic hearing loss.
Six TMPRSS3 variants were found to cosegregate in 10 consanguineous Pakistani families with autosomal recessive non-syndromic hearing impairment.
Data imply that TMPRSS3-A/D overexpression in EOC is probably due to hypomethylation of their control region.
TMPRSS3 gene is not a major contributor to non-syndromic deafness in the Moroccan population.
miR-204 has a role in suppressing cochlear spiral ganglion neuron survival in vitro by targeting TMPRSS3
Lack of Tmprss3 leads to a decrease in Kcnma1 potassium channels expression in cochlear inner hair cells.
The distribution of TMPRSS3 was observed in many regions of the mouse cochlea, but mainly in the spiral ganglion neurons.
Tmprss3 acts as a permissive factor for cochlear hair cells survival and activation at the onset of hearing and is required for saccular hair cell survival
This gene encodes a protein that belongs to the serine protease family. The encoded protein contains a serine protease domain, a transmembrane domain, an LDL receptor-like domain, and a scavenger receptor cysteine-rich domain. Serine proteases are known to be involved in a variety of biological processes, whose malfunction often leads to human diseases and disorders. This gene was identified by its association with both congenital and childhood onset autosomal recessive deafness. This gene is expressed in fetal cochlea and many other tissues, and is thought to be involved in the development and maintenance of the inner ear or the contents of the perilymph and endolymph. This gene was also identified as a tumor-associated gene that is overexpressed in ovarian tumors. Alternatively spliced transcript variants have been described.
transmembrane protease, serine 3
, transmembrane protease serine 3-like
, serine protease TADG-12
, transmembrane protease serine 3
, tumor-associated differentially-expressed gene 12 protein
, transmembrane proteinase serine 3