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the role of Lin28 in controlling developmental transitions is evolutionary conserved and establishes a functional interaction between Lin28 and thyroid hormone (show PTH Proteins) function.
It has been shown that the constitutive expression of Lin28a during neuronal differentiation in vitro positively and negatively affects numerous miRNAs.
ur study demonstrated that disturbance of the let-7/LIN28 double-negative feedback loop is involved in the regulation of radio- and chemo-resistance, and that let-7 and LIN28 could be employed as predictive biomarkers of response to radiotherapy or chemotherapy in non-small-cell lung cancer patients.
tight control by ESE3/EHF (show EHF Proteins) over the Lin28/let-7 axis is a critical barrier to malignant transformation.
MSI2 (show MSI2 Proteins) might play a crucial role in sustaining stemness and chemoresistance of liver cancer stem cells in LIN28A-dependent manner in hepatocellular carcinoma.
High LIN28A expression is associated with colorectal cancer.
LIN28A and LIN28B (show LIN28B Proteins) play cooperative roles in regulating reprogramming, naive/primed pluripotency, and stem cell metabolism.
The molecular dynamics simulations suggest that a conserved structural feature of the loop regions of pre-let-7 miRNAs is more important for LIN28 recognition than sequence conservation among members of the let-7 family or the presence of the GGAG motif in the 3' region.
Lin28A is up-regulated in 73.3 % of colon cancer patients. Lin28A-enforced expression in colon cancer cells enhanced the chemosensitivity of cancer cells to 5-FU via promoting apoptosis in a let-7 independent manner, associated with decreasing the expression of DNA damage repair protein H2AX.
Upregulation of let-7a carries the potential to reverse CCL18 (show CCL18 Proteins) induced cell proliferation and migration alteration in breast cancer cells by regulating Lin28 expression.
Data suggest that the Lin28/let-7 (lin-28 homolog protein/mirnlet7 microRNA) molecular switch plays roles in regulation of cell growth signaling pathways and in regulation of expression of metabolic enzymes. [REVIEW]
Lin28 pseudogenes do not acquire patterns of tissue-specific methylation as for the parental gene, but rather are methylated in patterns specific to the local genomic environment into which they were inserted.
Overexpression of LIN28A, which is a hallmark of human ETMRs, augments Sonic-hedgehog (Shh (show SHH Proteins)) and Wnt (show WNT2 Proteins) signaling in embryonal tumors with multilayered rosettes precursor cells through the downregulation of let7-miRNA, and LIN28A/let7a interaction with the Shh (show SHH Proteins) pathway was detected at the level of Gli (show GLI1 Proteins) mRNA.
During ESC differentiation, Lin28 transient induction is dependent on Otx2 and Hmga2 and prevents an inappropriate excessive rise of Hmga2 levels.-
MAPK/ERK (show MAPK1 Proteins) directly impacts LIN28, defining an axis that connects signalling, post-transcriptional gene control, and cell fate regulation.
Sirt1 (show SIRT1 Proteins) knockdown abolished the protective effects of Lin28a against cardiac remodeling and dysfunction after MI, and Lin28a failed to increase the numbers of GFP-LC3 (show MAP1LC3A Proteins)-positive punctae and decrease aggresome and p62 (show GTF2H1 Proteins) accumulation in Sirt1 (show SIRT1 Proteins)-knockdown neonatal cardiomyocytes subjected to hypoxia-induced injury.
data point toward a complex system of regulation by Lin28a, Lin28b (show LIN28B Proteins), and let-7, in which Lin28b (show LIN28B Proteins) and let-7 can impact both puberty and growth in a sex-specific manner
Lin28A binds active promoters and recruits Tet1 (show TET1 Proteins) to regulate gene expression via epigenetic DNA modifications.
Lin28a protects against DCM through PKA/ROCK2 (show ROCK2 Proteins) dependent pathway.
Lin28B (show LIN28B Proteins) upregulation in a mouse model does not affect neuroblast proliferation, ganglion size, and Let-7 expression during early postnatal development
Data show that the RNA-binding protein lin28a/microRNA let-7a axis regulated glucose metabolism in part through the insulin (show INS Proteins)-PI3K-mTOR (show FRAP1 Proteins) pathway.
The knockdown of Lin-28a or Lin-28b (show LIN28B Proteins) function by morpholino microinjection into embryos resulted in severe cell proliferation defects during early morphogenesis.
The Lin-28 is induced in Muller glia within 6 h following retinal injury and is necessary for Muller glia dedifferentiation.
Acts as a 'translational enhancer', driving specific mRNAs to polysomes and thus increasing the efficiency of protein synthesis. Its association with the translational machinery and target mRNAs results in an increased number of initiation events per molecule of mRNA and, indirectly, in stabilizing the mRNAs. Acts as a suppressor of microRNA (miRNA) biogenesis by specifically binding the precursor let-7 (pre-let-7), a miRNA precursor. Acts by binding pre-let-7 and recruiting an uridylyltransferase, leading to the terminal uridylation of pre- let-7. Uridylated pre-let-7 miRNAs fail to be processed by Dicer and undergo degradation. Specifically recognizes the 5'-GGAG-3' motif in the terminal loop of pre-let-7. Also recognizes and binds non pre-let-7 pre-miRNAs that contain the 5'-GGAG-3' motif in the terminal loop, leading to their terminal uridylation and subsequent degradation (By similarity).
, protein lin-28 homolog A
, lin-28 homolog
, RNA-binding protein LIN-28
, lin-28 homolog A (C. elegans)
, RNA-binding protein LIN-28A
, zinc finger CCHC domain-containing protein 1
, zinc finger, CCHC domain containing 1
, testis expressed gene 17
, testis-expressed protein 17
, RNA-binding protein lin-28