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The protein encoded by LIN28B 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. Additionally we are shipping LIN28B Antibodies (82) and many more products for this protein.
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LIN28A (show LIN28A Proteins) and LIN28B play cooperative roles in regulating reprogramming, naive/primed pluripotency, and stem cell metabolism.
The identification of the let-7/Lin28 (show LIN28A Proteins) axis as an important regulator of HSC (show FUT1 Proteins) activation as well as its upstream modulators and down-stream targets will provide insights into the involvement of altered microRNA expression in contributing to the pathogenesis of alcoholic liver fibrosis
the LIN28B rs221634 A>T polymorphism was associated with an increased neuroblastoma (show ARHGEF16 Proteins) risk in Southern Chinese children.
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 (show LIN28A Proteins) expression.
LIN28B orchestrates oncogenic signaling in neuroblastoma (show ARHGEF16 Proteins).
loss of SIRT6 (show SIRT6 Proteins) results in hyperacetylation of H3K9 and H3K56 at the promoter of the LIN28B gene, creating a more permissive chromatin state and allowing for the Myc (show MYC Proteins) transcription factor to drive its expression
Compared with NCMT samples from the same OSCC patient, the expression of Lin28B was increased in all of the tumor samples. A similar upregulation of Lin28B was also observed in LN metastatic when compared with local tumors.
suggest that molecular subtypes of the LIN-28B/let-7a/IGF-II axis associate with heterogeneous progression
let-7 disruption by LIN28B, MYCN (show MYCN Proteins) sponging, or genetic loss is a unifying mechanism of neuroblastoma (show ARHGEF16 Proteins) development with broad implications for cancer pathogenesis
elevated LIN28B expression as a hallmark of a novel fetal-like subgroup in Juvenile myelomonocytic leukemia.
Study generated transgenic mice that either overexpressed Lin28b in Math1 (show ATOH1 Proteins)-positive cerebellar granule neuron precursors or in a broad range of Nestin (show NES Proteins)-positive neural precursors; while overexpression of LIN28B in Nestin (show NES Proteins)-positive cells does not lead to tumor formation, it results in a protracted development of granule cells and inhibitory interneurons and leads to a hypersublobulation of the cerebellar vermis.
this study shows that ectopic Lin28b expression reinitiates fetal regenerative potential in a subset of adult hematopoietic stem cells
expression of the heterochronic factor Lin28b decreases in common myeloid progenitors during hematopoietic maturation to adulthood in mice.
loss of Lin28b expression in fetal T cells leads to increased mature let-7, which causes decreased expression of TGF-betaRI, TGF-betaRIII, and SMAD2 (show SMAD2 Proteins) proteins. A reduction in TGF-beta (show TGFB1 Proteins) signaling leads to reduced Treg numbers.
Lin28b positively regulates the expression of Lin28b itself and cell cycle-related proteins in hepatoblasts by suppressing the maturation of target microRNAs, lethal-7b and miR (show MLXIP Proteins)-125a/b, enabling maintenance of the stem cell properties of hepatoblasts.
data point toward a complex system of regulation by Lin28a (show LIN28A Proteins), Lin28b, and let-7, in which Lin28b and let-7 can impact both puberty and growth in a sex-specific manner
Lin28B/let-7 axis acts as a critical driver of peripheral nervous system myelination
These results implicate a key role for the LIN28B/let-7 axis in regulating postnatal supporting cell (show PTPRJ Proteins) plasticity.
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.
lin-28 homolog B (C. elegans)
, lin-28 homolog B
, protein lin-28 homolog B