KHDRBS3 interacts with splicing protein Sam68 and oncogene
metadherin in prostate cancer cells.[9]
Clinical significance
KHDRBS3 (T-STAR) expression has been shown to be increased in
prostate cancer tissue compared to the surrounding benign tissue.[9] Expression of KHDRBS3 correlates with
mpMRI signal measured through Likert score a system similar to
PI-RADS.[9] While still under debate, mpMRI signal correlates with higher
Gleason grade and tumour size, in addition to
histopathological features associated with clinically aggressive prostate cancer.[10][11] Expression of KHDRBS3 was increased in the failing human myocardium of
heart failure patients, here KHDRBS3 protein interacted with several important mRNAs coding for sarcomere components, such as actin gamma 1 (ACTG1), myosin light chain 2 (MYL2), ryanodine receptor 2 (RYR2), troponin I3 (TNNI3), troponin T2 (TNNT2), tropomyosin 1 (TPM1), tropomyosin 2 (TPM2), and titin (TTN).[12]
In prostate cancer cell lines KHDRBS3 appears to be androgen regulated, with a reduction in mRNA expression occurring following addition of synthetic androgen
R1881 to cells.[9]
Function
KHDRBS3 regulates the alternative
mRNA splicing of the
sacromere protein titin (
TTN), leading to
intron retention. Overexpression of KHDRBS3 in
induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) increased Ca2+ transient amplitude and resulted in an increase of Fmax.[12]
Sugimoto Y, Morita R, Amano K, Shah PU, Pascual-Castroviejo I, Khan S, et al. (August 2001). "T-STAR gene: fine mapping in the candidate region for childhood absence epilepsy on 8q24 and mutational analysis in patients". Epilepsy Research. 46 (2): 139–44.
doi:
10.1016/S0920-1211(01)00274-1.
PMID11463515.
S2CID28713407.
Kool J, van Zaane W, van der Eb AJ, Terleth C (November 2001). "Down-regulation of T-STAR, a growth inhibitory protein, after SV40-mediated immortalization". Cell Growth & Differentiation. 12 (11): 535–41.
PMID11714634.
KHDRBS3 interacts with splicing protein Sam68 and oncogene
metadherin in prostate cancer cells.[9]
Clinical significance
KHDRBS3 (T-STAR) expression has been shown to be increased in
prostate cancer tissue compared to the surrounding benign tissue.[9] Expression of KHDRBS3 correlates with
mpMRI signal measured through Likert score a system similar to
PI-RADS.[9] While still under debate, mpMRI signal correlates with higher
Gleason grade and tumour size, in addition to
histopathological features associated with clinically aggressive prostate cancer.[10][11] Expression of KHDRBS3 was increased in the failing human myocardium of
heart failure patients, here KHDRBS3 protein interacted with several important mRNAs coding for sarcomere components, such as actin gamma 1 (ACTG1), myosin light chain 2 (MYL2), ryanodine receptor 2 (RYR2), troponin I3 (TNNI3), troponin T2 (TNNT2), tropomyosin 1 (TPM1), tropomyosin 2 (TPM2), and titin (TTN).[12]
In prostate cancer cell lines KHDRBS3 appears to be androgen regulated, with a reduction in mRNA expression occurring following addition of synthetic androgen
R1881 to cells.[9]
Function
KHDRBS3 regulates the alternative
mRNA splicing of the
sacromere protein titin (
TTN), leading to
intron retention. Overexpression of KHDRBS3 in
induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) increased Ca2+ transient amplitude and resulted in an increase of Fmax.[12]
Sugimoto Y, Morita R, Amano K, Shah PU, Pascual-Castroviejo I, Khan S, et al. (August 2001). "T-STAR gene: fine mapping in the candidate region for childhood absence epilepsy on 8q24 and mutational analysis in patients". Epilepsy Research. 46 (2): 139–44.
doi:
10.1016/S0920-1211(01)00274-1.
PMID11463515.
S2CID28713407.
Kool J, van Zaane W, van der Eb AJ, Terleth C (November 2001). "Down-regulation of T-STAR, a growth inhibitory protein, after SV40-mediated immortalization". Cell Growth & Differentiation. 12 (11): 535–41.
PMID11714634.