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TMPRSS2 encodes a protein that belongs to the serine protease family. Additionally we are shipping TMPRSS2 Antibodies (65) and TMPRSS2 Kits (14) and many more products for this protein.
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Studies showed that urinary TMPRSS2:ERG (show ERG Proteins) transcripts seem to be indicative of Prostate cancer aggressiveness upon biopsy. [review]
Aspirin was associated with a significant reduction in the relative risk of TMPRSS2:ERG (show ERG Proteins) (T2E )fusion positive, but not T2E negative
the type II transmembrane serine protease (show TMPRSS11E Proteins) TMPRSS2 was able to activate hemagglutinin (show HA Proteins) for cell entry indicating that bat (show BAAT Proteins) influenza A virus can utilize human proteases for hemagglutinin (show HA Proteins) activation.
The relatively low rate of ERG (show ERG Proteins)-positive prostatic intraepithelial neoplasia counts in favor of the limited role of chimeric transcript TMPRSS2/ERG (show ERG Proteins) in the differential diagnosis of prostatic intraepithelial neoplasia
TMPRSS2 isoform 1 is expressed in viral target cells.
The TMPRSS2-ERG (show ERG Proteins) Gene Fusion Blocks XRCC4 (show XRCC4 Proteins)-Mediated Nonhomologous End-Joining Repair and Radiosensitizes Prostate Cancer Cells to PARP Inhibition
The potential for TMPRSS2:ERG gene fusion, detected by IHC, to modify the role of PTEN loss in lethal progression of prostate cancer.
Results indicate that PTEN loss occurs in cooperation with TMPRSS2-ERG fusion in prostate cancer and the majority of the samples harbor TMPRSS2-ERG fusion as well as PTEN gene deletion.
Elucidation of ERG (show ERG Proteins) regulation of ABEs in castration-resistant prostate cancer (CRPC) may help to stratify TMPRSS2-ERG fusion-positive prostate cancer patients in the clinic for anti-androgen receptor (show AR Proteins)-driven therapies.
these data show that the androgen-driven events causing TMPRSS2-ERG (show ERG Proteins) fusions and other rearrangements of androgen-dependent genes in prostate epithelial cells of young patients preferentially lead to low-grade (and not high-grade) prostate cancer.
Genetic inhibition of TMPRSS2-ERG (show ERG Proteins) junction oncogene (show RAB1A Proteins) in prostate cancer by means of siRNA has strong antineoplastic effect in a mouse model and in vitro.
The androgen-regulated protease TMPRSS2 activates a proteolytic cascade involving components of the tumor microenvironment and promotes prostate cancer metastasis
TMPRSS2 as a host cell factor essential for viral spread and pathogenesis of mono-basic H1N1 and H3N2 influenza A viruses.
These results demonstrate that TMPRSS2 expression is essential for influenza A virus replication in vivo.
These data demonstrate that TMPRSS2 is a host factor that is essential for pneumotropism and pathogenicity of H7N9 and H1N1 influenza virus in mice.
Loss of TMPRSS2 serine protease (show F2 Proteins) activity does not influence fertility, reduce survival, result in prostate hyperplasia or carcinoma, or alter prostatic luminal epithelial cell regrowth following castration and androgen replacement.
This gene encodes a protein that belongs to the serine protease family. The encoded protein contains a type II transmembrane domain, a receptor class A domain, a scavenger receptor cysteine-rich domain and a protease domain. Serine proteases are known to be involved in many physiological and pathological processes. This gene was demonstrated to be up-regulated by androgenic hormones in prostate cancer cells and down-regulated in androgen-independent prostate cancer tissue. The protease domain of this protein is thought to be cleaved and secreted into cell media after autocleavage. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, serine protease 10
, transmembrane protease serine 2
, plasmic transmembrane protein X