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Human Polyclonal PCGF2 Primary Antibody pour ELISA, WB - ABIN249894
Ishida, Asano, Hasegawa, Koseki, Ono, Yoshida, Taniguchi, Kanno: Cloning and chromosome mapping of the human Mel-18 gene which encodes a DNA-binding protein with a new 'RING-finger' motif. dans Gene 1993
Low expression of Mel-18 is correlated with gastric cancer.
Suggest a novel role of PCGF2 in arsenic trioxide-mediated degradation of PML-RARA that PCGF2 might act as a negative regulator of UBE2I via direct interaction.
Mel-18 underexpression in luminal breast cancer cells caused ER-alpha downregulation.Its overexpression restored it in triple-negative breast cancer cells. MEL-18 suppressed SUMOylation of the ESR1 transactivators p53 and SP1.
It was therefore concluded that the lower Mel-18 expression might contribute to colorectal cancer development/progression.
Mel-18 functions as a tumor suppressor by its novel negative control of the epithelial-mesenchymal transition in breast cancer.
Findings suggest that Mel-18 is a novel negative regulator of breast cancer stem cell (CSC) that inhibits the stem cell population and in vitro and in vivo self-renewal through the inactivation of Wnt-mediated Notch signaling.
PCGF2, a PRC1 gene, played a negative role in the granulocytic differentiation of human APL cells.
these findings provide that Mel-18 is a novel regulator of tumor angiogenesis through regulating HIF-1alpha and its target VEGF expressions mediated by the PTEN/PI3K/Akt pathway, suggesting a new tumor-suppressive role of Mel-18 in human breast cancer.
Loss of Mel-18 is associated with prostate cancer.
Our analysis showed correlation between BMI1 and PCGF2 gene's expression and survival in children with medulloblastoma.
Bmi-1/Mel-18 ratio can be potentially used as a tool for stratifying women at risk of developing breast malignancy.
Mel-18 may serve as a useful marker in prognostic evaluation for patients with breast cancer.
Decreased Mel-18 and increased Bmi-1 mRNA expression was associated with the carcinogenesis and progression of gastric cancer
An association of Mel18 with emerin was observed in Hutchinson-Gilford progeria syndrome, but not in WT cells.
Mel-18 plays a significant role in the angiogenic function of endothelial cells by regulating endothelial gene expression.
BMI1 acts as an oncogene and Mel-18 functions as a tumor suppressor via downregulation of BMI1.
The oncogenic role of MEL-18 in human primary breast carcinomas is determined by its capacity to inhibit INK4a/ARF proteins(p16INK4a, p14ARF, or h-TERT) or to induce telomerase activity.
Our data suggest that Mel-18 regulates Bmi-1 expression during senescence via down-regulation of c-Myc.
These results suggest that Bmi-1 and Mel-18 may have overlapping functions in cancer cell growth.
Mel-18 and Bmi-1 may regulate the Akt pathway in breast cancer cells, and that Mel-18 functions as a tumor suppressor by repressing the expression of Bmi-1 and consequently down-regulating Akt activity.
BMI1 and MEL18 contribute to the development of colitis-associated cancer in mice by promoting proliferation and reducing apoptosis via suppressing expression of Reg3b. REG3B negatively regulates cytokine-induced activation of STAT3 in colon epithelial cells.
Data indicate that Bmi1 and Mel18 have opposing functions and are present in distinct complexes.
Mel-18 controls the enrichment of tumor-initiating cells in side population fraction in mouse mammary gland cancer.
Data show that Mel-18 and Ezh2 positively regulate the expression of Il17a and Il17f.
Chemokine-mediated thymopoiesis is regulated by a mammalian Polycomb group gene, mel-18
involved in the specification of the anterior-posterior axis in mice
the stoichiometry and/or equilibrium of subunits of the class II Polycomb complex containing Mel-18 might be regulated by changes in phosphorylation status via the PKC signaling pathway
Results provide genetic evidence that Cited2 controls the expression of INK4a/ARF and fibroblast proliferation, at least in part via the polycomb-group genes Bmi1 and Mel18.
Loss or knockdown of mel-18 leads to the expression of Hoxb4, an increase in the proportion of hematopoietic stem cells in G0 phase, and the subsequent promotion of HSC self-renewal.
Mel-18 contributes to the maintenance of the active state of the Hes-1 gene as a cellular memory system, thereby supporting the expansion of early T lymphocyte progenitors.
Sf3b1-Zfp144 protein interaction is essential for true Polycomb group proteins mediated repression of Hox genes.
observed that expression of the PcG genes-bmi1 and mel-18-is correlated with self-renewal and differentiation of HSCs. Thus, it was suggested that the balance between Bmi1 and Mel-18 regulates self-renewal of HSCs
The protein encoded by this gene contains a RING finger motif and is similar to the polycomb group (PcG) gene products. PcG gene products form complexes via protein-protein interaction and maintain the transcription repression of genes involved in embryogenesis, cell cycles, and tumorigenesis. This protein was shown to act as a negative regulator of transcription and has tumor suppressor activity. The expression of this gene was detected in various tumor cells, but is limited in neural organs in normal tissues. Knockout studies in mice suggested that this protein may negatively regulate the expression of different cytokines, chemokines, and chemokine receptors, and thus plays an important role in lymphocyte differentiation and migration, as well as in immune responses.
polycomb group RING finger protein 2
, zinc finger protein 144 (Mel-18) (human homolog)
, polycomb group ring finger 2
, ring finger protein 110
, DNA-binding protein Mel-18
, zinc finger protein 144
, melanoma nuclear protein 18