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In vitro, uremia induced dysregulation of DNA methylation in differentiating monocytes, which affected several transcription regulators important for monocyte differentiation (e.g., FLT3, HDAC1, MNT) and led to enhanced generation of intermediate monocytes.
SPAG9 (show SPAG9 Proteins) mRNA and protein overexpression in lung cancer tissue, and the presence of SPAG9 (show SPAG9 Proteins) IgG antibody in peripheral blood of lung cancer patients indicates that it has potential as a biomarker for lung cancer diagnosis.
SPAG9 (show SPAG9 Proteins)-elevated expression contributes to malignant behavior and poor prognosis of breast cancer and may support a potential indicator in treatment selection.
Study suggest that suppression of miR (show MLXIP Proteins)-141 may cause an aberrant overexpression of SPAG9 (show SPAG9 Proteins) promoting growth and metastasis of hepatocellular carcinoma cells.
expression of SPAG9 (show SPAG9 Proteins) in ECC cells with TGF-beta1 (show TGFB1 Proteins) treatment and spheroids formation was increased
PLK1 binding to JIP4 (show SPAG9 Proteins) was found in G2 phase and mitosis, and PLK1 binding was self-primed by PLK1 phosphorylation of JIP4 (show SPAG9 Proteins).
Based on in vitro assays, we found miR (show MLXIP Proteins)-200a-3p significantly inhibit cancer cell proliferation by inducing apoptosis.
FOXK1 protein levels and activity are regulated by associating with JLP and PLK1
SPAG9 (show SPAG9 Proteins) overexpression in gastric cancer correlates with poor prognosis and contributes to gastric cancer cell proliferation
Here we review the activities of MYC (show MYC Proteins), MNT and other MAX interacting proteins in the setting of T and B cell activation (show BLNK Proteins) and oncogenesis
results redefine the physiological relationship between Mnt and Myc (show MYC Proteins) and requirements for Myc (show MYC Proteins)-driven oncogenesis
Mxd4 (show MXD4 Proteins) and Mnt upregulation following OX40 (show TNFRSF4 Proteins) engagement most likely increases T-cell survival
There is a unique negative regulatory role for Mnt in governing key Myc (show MYC Proteins) functions associated with cell proliferation and tumorigenesis.
Mnt may serve a general role as a Myc (show MYC Proteins) antagonist.[Review]
Mnt represses Myc target genes and Myc functions as an oncogene by relieving Mnt-mediated repression
Loss of protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects.
These results demonstrate that Mnt-Myc (show MYC Proteins) antagonism plays a fundamental role in regulating cell cycle entry and proliferation.
Mnt is expressed both in growth-arrested and proliferating mouse fibroblasts and is phosphorylated when resting cells are induced to re-enter the cell cycle
Mnt functions as a tumor suppressor and reveal a critical and surprising role for Mnt in the regulation of T-cell development and in T-cell-dependent immune homeostasis.
The switch from Mnt-Max to Myc (show MYC Proteins)-Max during bile duct ligation (cholestasis) and in hepatocytes treated with lithocholic acid is responsible for the induction in p53 (show TP53 Proteins) and cyclin D1 (show CCND1 Proteins) expression and contributes to apoptosis.
The Myc/Max/Mad network comprises a group of transcription factors that co-interact to regulate gene-specific transcriptional activation or repression. This gene encodes a protein member of the Myc/Max/Mad network. This protein has a basic-Helix-Loop-Helix-zipper domain (bHLHzip) with which it binds the canonical DNA sequence CANNTG, known as the E box, following heterodimerization with Max proteins. This protein is likely a transcriptional repressor and an antagonist of Myc-dependent transcriptional activation and cell growth. This protein represses transcription by binding to DNA binding proteins at its N-terminal Sin3-interaction domain.
C-Jun-amino-terminal kinase-interacting protein 4
, JNK interacting protein
, JNK/SAPK-associated protein
, Max-binding protein
, c-Jun NH2-terminal kinase-associated leucine zipper protein
, cancer/testis antigen 89
, human lung cancer oncogene 6 protein
, lung cancer oncogene 4
, mitogen-activated protein kinase 8-interacting protein 4
, proliferation-inducing gene 6
, protein highly expressed in testis
, sperm surface protein
, sunday driver 1
, MAX binding protein
, Max-interacting protein
, class D basic helix-loop-helix protein 3
, max-binding protein MNT
, myc antagonist MNT
, max binding protein