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Human Polyclonal LIN28A Primary Antibody for ICC, IF - ABIN4331040
Boj, Hwang, Baker, Chio, Engle, Corbo, Jager, Ponz-Sarvise, Tiriac, Spector, Gracanin, Oni, Yu, van Boxtel, Huch, Rivera, Wilson, Feigin, Öhlund, Handly-Santana, Ardito-Abraham, Ludwig, Elyada et al.: Organoid models of human and mouse ductal pancreatic cancer. ... in Cell 2015
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Human Monoclonal LIN28A Primary Antibody for ICC, ELISA - ABIN968936
Gerecht-Nir, Dazard, Golan-Mashiach, Osenberg, Botvinnik, Amariglio, Domany, Rechavi, Givol, Itskovitz-Eldor: Vascular gene expression and phenotypic correlation during differentiation of human embryonic stem cells. in Developmental dynamics : an official publication of the American Association of Anatomists 2005
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ectopic expression of human Lin28A has the same effect as Drosophila Lin-28, indicating functional conservation in Lin-28 orthologs
Data suggest that overexpression of Linc00662 enhances lung cancer cell metastasis and cancer stem cell characteristics; these characteristics seem to involve interaction of Linc00662 with LIN28 in lung cancer cells; lung cancer patients with higher Linc00662 expression levels exhibit lower overall survival rate than patients with lower Linc00662 expression levels. (LINC00662 = long intergenic non-protein coding RNA 662)
LIN28 is a very specific marker (98% specificity) for distinguishing classic gastric hepatoid carcinomas from hepatocellular carcinoma
Data indicated that LIN28A might make contribution to HSF proliferation and extracellular matrix synthesis upon thermal injury.
LIN28A inhibits lysosomeassociated membrane glycoprotein 1 protein expression in embryonic stem and bladder cancer cells.
Studied effects of lin-28 homolog A protein (Lin28A) on cells proliferation, migration, invasion and apoptosis of osteocarcinoma (OS) cells through metastasis associated lung adenocarcinoma transcript 1 (MALAT1).
Pig induced pluripotent stem cell (piPSC) line was generated from embryonic fibroblast cells using retroviral transduction approaches carrying human transcriptional factors: OCT4, SOX2, KLF4, c-MYC and LIN28.
LIN28A is a sensitive IHC marker for the diagnosis of Embryonal Tumor with Multilayered Rosettes , but immunoreactivity can also be seen in a proportion of Atypical Teratoid/Rhabdoid Tumors
Recent improvement in high-throughput sequencing has highlighted the potential role of LIN28/let-7 regulatory network in several developmental events. It was proposed that this pathway might represent a functional signature in cell proliferation, transition between commitment and pluripotency, and regulation of cancer and tumorigenicity.
Knockdown of miR-128a induces Lin28a expression and reverts myeloid differentiation blockage in acute myeloid leukemia.
Lin28A and Lin28B are co-expressed colon cancer tissues and have functional similarities.
this study demonstrates that Lin28A can activates androgen receptor via regulation of c-myc and promotes malignancy of ER-/Her2+ breast cancer
The results suggest that the Lin28a gene enhances the osteoblastic differentiation of human periosteum-derived cells. In addition, the Lin28a gene increases mitochondrial activity in human periosteum-derived cells.
High LIN28A expression is associated with pancreatic cancer.
the specific interaction between zinc knuckle domain of LIN28 and pre-let-7 is necessary and sufficient to induce oligouridylation.
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 over the Lin28/let-7 axis is a critical barrier to malignant transformation.
MSI2 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.
Overexpression of Lin28a, an RNA-binding protein that regulates organismal growth and metabolism, in articular chondrocyte progenitor cells upregulated Erk signaling and increased articular cartilage thickness.
The apoptotic protection by Lin28a inhibition is likely through the activation of TrkA signaling pathway.
In the absence of Eprn, Lin28a expression is reduced which results in persistence of let-7 microRNAs, and the up-regulation of de novo methyltransferases Dnmt3a/b is delayed. Dnmt3a/b deletion retards ES cell transition, correlating with delayed Nanog promoter methylation and phenocopying loss of Eprn or Lin28a.
miR-145 modulation of Sox2-Lin28/let-7 network is crucial for neurogenesis progression.
The results reveal a key role of Wnt-Lin28-let7 miRNA signaling in regulating proliferation and neurogenic potential of Muller glial cells in the adult mammalian retina.
LIN28 specifically marks undifferentiated spermatogonia in mice. The LIN28-expressing undifferentiated spermatogonia exist as two subpopulations: Ngn3-GFP-negative (high stem cell potential) and Ngn3-GFP-positive (high differentiation commitment)
Overexpression of LIN28A, which is a hallmark of human ETMRs, augments Sonic-hedgehog (Shh) and Wnt signaling in embryonal tumors with multilayered rosettes precursor cells through the downregulation of let7-miRNA, and LIN28A/let7a interaction with the Shh pathway was detected at the level of Gli mRNA.
During ESC differentiation, Lin28 transient induction is dependent on Otx2 and Hmga2 and prevents an inappropriate excessive rise of Hmga2 levels.-
LIN28A and LIN28B play cooperative roles in regulating reprogramming, naive/primed pluripotency, and stem cell metabolism.
MAPK/ERK directly impacts LIN28, defining an axis that connects signalling, post-transcriptional gene control, and cell fate regulation.
Sirt1 knockdown abolished the protective effects of Lin28a against cardiac remodeling and dysfunction after MI, and Lin28a failed to increase the numbers of GFP-LC3-positive punctae and decrease aggresome and p62 accumulation in Sirt1-knockdown neonatal cardiomyocytes subjected to hypoxia-induced injury.
data point toward a complex system of regulation by Lin28a, Lin28b, and let-7, in which Lin28b and let-7 can impact both puberty and growth in a sex-specific manner
Lin28A binds active promoters and recruits Tet1 to regulate gene expression via epigenetic DNA modifications.
Lin28a protects against DCM through PKA/ROCK2 dependent pathway.
Lin28B 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-PI3K-mTOR pathway.
Lin28a protects against hypoxia/reoxygenation induced cardiomyocytes apoptosis by alleviating mitochondrial dysfunction under high glucose/high fat conditions
Lin28a overexpression efficiently and specifically reduces let-7 miRNAs and up-regulates let-7 target genes.
the role of Lin28 in controlling developmental transitions is evolutionary conserved and establishes a functional interaction between Lin28 and thyroid hormone function.
The knockdown of Lin-28a or Lin-28b 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.
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.
Dual-luciferase reporter assay validated that miR-370, one of the 16 common microRNAs, could directly target the 3'UTR of LIN28A.
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).
RNA-binding protein LIN-28
, protein lin-28 homolog A
, 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-28A
, RNA-binding protein lin-28
, lin-28 homolog A (C. elegans)