Human Gene LIN28B (uc003pqv.2) Description and Page Index
Description: Homo sapiens lin-28 homolog B (C. elegans) (LIN28B), mRNA. RefSeq Summary (NM_001004317): The protein encoded by this gene belongs to the lin-28 family, which is characterized by the presence of a cold-shock domain and a pair of CCHC zinc finger domains. This gene is highly expressed in testis, fetal liver, placenta, and in primary human tumors and cancer cell lines. It is negatively regulated by microRNAs that target sites in the 3' UTR, and overexpression of this gene in primary tumors is linked to the repression of let-7 family of microRNAs and derepression of let-7 targets, which facilitates cellular transformation. [provided by RefSeq, Jun 2012]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Gene record to access additional publications. ##Evidence-Data-START## Transcript exon combination :: DQ127228.1, BC137526.1 [ECO:0000332] RNAseq introns :: single sample supports all introns SAMEA1968968, SAMEA2142853 [ECO:0000348] ##Evidence-Data-END## ##RefSeq-Attributes-START## MANE Ensembl match :: ENST00000345080.5/ ENSP00000344401.4 RefSeq Select criteria :: based on conservation ##RefSeq-Attributes-END## Transcript (Including UTRs) Position: hg19 chr6:105,404,923-105,531,207 Size: 126,285 Total Exon Count: 4 Strand: + Coding Region Position: hg19 chr6:105,405,126-105,526,658 Size: 121,533 Coding Exon Count: 4
ID:LN28B_HUMAN DESCRIPTION: RecName: Full=Protein lin-28 homolog B; Short=Lin-28B; FUNCTION: 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 ZCCHC11/TUT4 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. Mediates MYC-mediated let-7 repression. Isoform 1, when overexpressed, stimulates growth of the breast adenocarcinoma cell line MCF-7. Isoform 2 has no effect on cell growth. SUBUNIT: Interacts with ZCCHC11/TUT4. SUBCELLULAR LOCATION: Cytoplasm. Nucleus. Note=Predominantly cytoplasmic at G1 phase, accumulates in the nucleus in S and G2 phases. The frequency of nuclear localization in S and in G2 phases is 60% and 30%, respectively. TISSUE SPECIFICITY: High expression in testis, fetal liver, placenta and in hepatocellular carcinoma (HCC). Isoform 1 is only detected in moderately and poorly differentiated HCC tissues and placenta (at protein level). Isoform 2 is detected in fetal liver, non-tumor liver tissues, as well as well-differentiated tumor tissues (at protein level). INDUCTION: Might be negatively regulated by the microRNA let-7b. MISCELLANEOUS: Overexpressed in primary tumors (overall frequency approximately 15%), overexpression being linked to repression of let-7 family miRNAs and derepression of let-7 targets. Facilitates cellular transformation in vitro, and overexpression is associated with advanced disease across multiple tumor types. SIMILARITY: Belongs to the lin-28 family. SIMILARITY: Contains 2 CCHC-type zinc fingers. SIMILARITY: Contains 1 CSD (cold-shock) domain.
Genetic Association Studies of Complex Diseases and Disorders
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q6ZN17
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.