Tpm1T-Cell Phenotype Modifier 1
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miRNAs Blanco asociado Funcion del miRNA en metastasis de tumor miR-10b HOXD10 Promotor miR-21 PTEN, PDCD4, TPM1, Maspin Promotor miR-373 CD44, LATS2 Promotor miR-520c CD44 Promotor miR-155 RhoA Promotor Let-7 Ras, HMGA2 Represor miR-335 SOX4, TNC Represor miR-126 Crk, IRS-1 Represor miR-146a ROCK1 Represor miR-101 EZH2 Represor Familia miR-200 ZEB1, ZEB2 Represor
1###Tropomyosin-1 alpha chain (TPM1)###gi|20522240 (Mouse)###5.3/39300###4.69 / 32661###476###22/ 36
Figure 1 illustrates the pattern of alternative splicing of the two sarcomeric TPM1 isoforms.
Security features include TPM1.2 data security technology, BIOS built-in security, and a Kensington lock connector.
Category Group Regulated core genes Cardiac hypertrophy WB TPM1.FGF23 Cardiac hypertrophy Imipramine EPO, UCN2, TERT, VDR, ACE Cardiac arrhythmia lmipramine ATP1A3, SCN1A, KCNH7, KCNG2, KCNQ1, ADORA1, ADRA1B, ADRB3, ADRA1D Cardiac adenopathy EtOH-Fr DLCAP4, MTHFS, EVC2, MAPK9.
miR-21 has been shown to promote tumorigenesis and metastasis through suppressing expression of PTEN, PDCD4, TPM1 and Maspin, being all negative regulators of both growth and migration and invasion (45-48).
Previous studies have shown that miR-21 interrnpts the activity of two tumor suppressor genes, PTEN (for phosphatase and tensin homolog) and TPM1 (tropomyosin 1).
These effects are probably associated with multiple tumor suppressor genes' concurrent downregulation throughout the various stages of tumor progression, including PDCD4, TPM1, maspin, and PTEN [20, 45].
(32) The remaining proteins, specifically TPM1, ACTB, ACTN4, LMNA, and TUBB, are important elements in the formation of the cytoskeleton itself.
Forced expression of miR-21 increases proliferation and invasion of PDAC cell lines, and this appears to occur through target inhibition of the phosphatase and tensin homolog (PTEN), programmed cell death 4 (PDCD4), presence of tropomyosin 1 (TPM1), and tissue inhibition of metalloproteinases-3 (TIMP3), thereby indirectly inducing expression of matrix metalloproteinase-2 and -9 and vascular endothelial growth factor (VEGF).
miR-21 is significantly upregulated in highly metastatic TSCC cell lines and metastatic tissues, and the level of miR-21 is inversely correlated with tropomyosin 1 (TPM1) and phosphatase and tensin homologue deleted on chromosome ten (PTEN) expression and TSCC cell apoptosis [15].