anti-Lin-28 Homolog B (C. Elegans) (LIN28B) Anticorps

Human Lin-28 Homolog B (C. Elegans) (LIN28B) interaction partners

1. Study provides evidence that cancer-testis (CT) genes LIN28B and was activated in lung adenocarcinoma (LUAD) patients. Its high expression is significantly associated with LUAD worse overall survival. Also, LIN28B promotes tumor proliferation and metastasis in vitro and in vivo.

2. LIN28B was a direct target of miR-26a in ambient particulate matter-bound metal-triggered lung cancer.

3. UFC1 has a promoting role in GC progression, at least in part, by acting as a miR-498 sponge and derepressing Lin28b expression, which would provide a novel biomarker for GC diagnosis and prognosis and offer a potential target for GC therapy.

4. Study investigated the effects of LIN28B expression on lung tumorigenesis using LIN28B transgenic overexpression in an autochthonous KRAS(G12V)-driven mouse model. LIN28B accelerates tumor initiation and enhances cell proliferation leading to a shortened overall survival. In addition, LIN28B expression is found in 24% of KRAS-mutated cases.

5. Study demonstrates the differential antagonistic functions of the LIN28B-short isoform against the LIN28B-long isoform through an inability to degrade LET-7, which leads to the novel premise that the short isoform may serve to counterbalance the long isoform during normal colonic epithelial homeostasis.

6. In colon cancer cells, up-regulation of LIN28B increased BCL-2 expression, enhanced its stability and reduced its ubiquitination.

7. Lin28B could facilitate gastric cancer stemness.

8. downregulation of Lin28b by miR-125a partially accounts for its antiproliferative activity toward hepatocellular carcinoma cells.

9. The effects of acetylated Lin28B on let-7a-1 and let-7g are similar to that of stable knockdown of Lin28B in H1299 cells. The new role of PCAF in mediating Lin28B acetylation and the specific release of its target microRNAs in H1299 cells may shed light on the potential application of let-7 in the clinical treatment of lung cancer patients

10. High LIN28B is associated with cervical cancer.

11. Data found that LIN28B expression is inhibited in hepatoma cells by miR-125b-5p promoting HBV replication.

12. Studied the association between Lin28 homolog B (LIN28B) gene polymorphisms and Wilms tumor susceptibility in Chinese children.

13. C allele frequency in rs314276 of LIN28B is associated with Central precocious puberty.

14. Testing for a combination of elevated IMP3 and Lin28B levels could further facilitate the identification of a patient subgroup with the worst ovarian cancer prognosis.

15. Lin28A and Lin28B are co-expressed colon cancer tissues and have functional similarities.

16. LIN28B is over-expressed in specific subtypes of pediatric leukemia and regulates lncRNA H19.

17. The study deciphered the essential role of Lin28B in the pathogenesis of epithelial-mesenchymal transition in idiopathic pulmonary fibrosis, and unraveled a novel mechanism that miR-26a is a modulator of let-7d.

18. Targeting LIN28B in acute myeloid leukemia cells resulted in cell cycle arrest, inhibition of cell proliferation and colony formation, which was induced by de-repression of let-7a miRNA. On the other hand, overexpression of LIN28B promoted cell proliferation.

19. common genetic variations (rs7759938 and rs314280) of LIN28B may contribute to idiopathic central precocious puberty susceptibility in Chinese girls

20. these findings reveal that lncRNA H19, miRNA let-7 and transcriptional factor LIN28 form a double-negative feedback loop, which has a critical role in the maintenance of breast cancer stem cells.

Mouse (Murine) Lin-28 Homolog B (C. Elegans) (LIN28B) interaction partners

1. Lin28b/let-7 axis controls the duration of kidney development

2. Regulating the IL-1beta/miR-i101/Lin28B signaling pathway.

3. The study deciphered the essential role of Lin28B in the pathogenesis of epithelial-mesenchymal transition in idiopathic pulmonary fibrosis, and unraveled a novel mechanism that miR-26a is a modulator of let-7d.

4. Study generated transgenic mice that either overexpressed Lin28b in Math1-positive cerebellar granule neuron precursors or in a broad range of Nestin-positive neural precursors; while overexpression of LIN28B in Nestin-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.

5. this study shows that ectopic Lin28b expression reinitiates fetal regenerative potential in a subset of adult hematopoietic stem cells

6. expression of the heterochronic factor Lin28b decreases in common myeloid progenitors during hematopoietic maturation to adulthood in mice.

7. 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 proteins. A reduction in TGF-beta signaling leads to reduced Treg numbers.

8. 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-125a/b, enabling maintenance of the stem cell properties of hepatoblasts.

9. LIN28A and LIN28B play cooperative roles in regulating reprogramming, naive/primed pluripotency, and stem cell metabolism.

10. The identification of the let-7/Lin28 axis as an important regulator of HSC 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

11. 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

12. Lin28B/let-7 axis acts as a critical driver of peripheral nervous system myelination

13. These results implicate a key role for the LIN28B/let-7 axis in regulating postnatal supporting cell plasticity.

14. Upregulation of LIN28B is associated with systemic mastocytosis.

15. Lin28a and Lin28b have overlapping functions in temporally regulating neural progenitor cell proliferation during early brain development.

16. VH repertoire of Lin28b-induced BM B1a B cells differs from that of normal B1a, suggesting persisting differences from fetal progenitors.

17. Our data imply dual repression of Let-7 during oocyte-embryo transition in the mouse model, the selective suppression of Let-7 biogenesis by Lin28 homologs superimposed on previously reported global suppression of miRNA activity.

18. Data implicate fetal expression of Lin28a/b in the regulation of life-long effects on metabolism and growth.

19. MYCN/LIN28B/Let-7/HMGA2 pathway implicated by meta-analysis of GWAS in suppression of post-natal proliferation thereby potentially contributing to aging

20. intestine targeted expression of LIN28B causes intestinal hypertrophy, crypt expansion, and Paneth cell loss