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NDRG2 is a member of the N-myc downregulated gene family which belongs to the alpha/beta hydrolase superfamily. Additionally we are shipping NDRG2 Antibodies (96) and NDRG2 Proteins (24) and many more products for this protein.
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NDRG2 is a novel ERS-responsive protein and acts as PERK co-factor to facilitate PERK branch, thereby contributing to ERS-induced apoptosis.
Our results show how NDRG2 expression serves as a critical determinant of the invasive and metastatic capacity of oral squamous cell carcinoma (OSCC)
Using double knockout of NDR1 (show STK38 ELISA Kits) and 2 shows that NDRs acted downstream of MST1 (show MST1 ELISA Kits) to mediate the egress of mature thymocytes from the thymus, as well as the interstitial migration of naive T cells within popliteal lymph nodes.
The expression level of NDRG2 has a causal influence on mood-related phenotypes.
Ndr1 (show STK38 ELISA Kits)/2-double null embryos show defects in somitogenesis and cardiac looping, which reveals their essential functions and shows that the NDR (show STK38 ELISA Kits) kinases are critically required during the early phase of organogenesis
Taken together, our results suggest that the expression of NDRG2 potentially inhibits osteoclast differentiation and plays a role in modulating the signal transduction pathway responsible for osteoclastogenesis.
NDRG2 is associated with decidualization during early pregnancy.
NDRG2 accumulated in skeletal muscle and myoblasts in the absence of TRIM32 (show TRIM32 ELISA Kits). NDRG2 overexpression in myoblasts led to reduced cell proliferation and delayed cell cycle withdrawal during differentiation.
Electroacupuncture administration can alleviate reference memory deficits and suppress N-myc downstream-regulated gene 2 upregulation in an AD transgenic mouse model
Rassf5 (show RASSF5 ELISA Kits) and Ndr1 (show STK38 ELISA Kits) or Ndr2 kinases regulate neuronal polarity through Par3 (show F2RL2 ELISA Kits) phosphorylation.
putative tumor suppressive function of NDRG2 may be confined to luminal- and basal B-type breast cancers
Overexpression of NDRG2 can inhibit the proliferation.
present results suggest that hypermethylation in promoter around exon 2 is functioning as essential factors of NDRG2 silencing in gastrointestinal cancers
NDRG2 overexpression significantly reduced hepatoma cell proliferation and enhanced cell apoptosis under glucose limitation. Moreover, NDRG2 overexpression aggravated energy imbalance and oxidative stress by decreasing the intracellular ATP and NADPH (show NQO1 ELISA Kits) generation and increasing ROS (show ROS1 ELISA Kits) levels.
The methylation status of the NDRG2 promoter in PBMCs is a potential noninvasive biomarker to predict the severity of liver fibrosis.
Data show that downregulation of NDRG2 may play an important role in advanced hepatoblastomas.
Study shows that NDRG2 was significantly down-regulated in glioblastomas (GBM) and seems to play a role in GBM prognosis. The low expression of NDRG2 at the mRNA level leads to a longer progression-free survival independent of methylation status.
Stuidies indicate the potential of N-myc downstream-regulated gene 2 (NDRG2) as a therapeutic target for cancer.
This gene is a member of the N-myc downregulated gene family which belongs to the alpha/beta hydrolase superfamily. The protein encoded by this gene is a cytoplasmic protein that may play a role in neurite outgrowth. This gene may be involved in glioblastoma carcinogenesis. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined.
, NDRG family member 2
, N-myc downstream-regulated gene 2
, N-myc downstream regulated 2
, N-myc downstream-regulated gene 2 protein
, protein Ndr2
, N-myc downstream regulator 2
, NDR1-related protein NDR2
, cytoplasmic protein Ndr1
, syld709613 protein
, N-myc downstream regulated gene 2
, NDRG1-related protein
, antidepressant-related protein ADRG123
, N-Myc downstream regulated gene 2