抗Human DAB2IP 抗体:
抗Rat (Rattus) DAB2IP 抗体:
抗Mouse (Murine) DAB2IP 抗体:
Human Polyclonal DAB2IP Primary Antibody for IP, WB - ABIN440620
Cook, Kim, Terao, Gotoh, Higuchi: Consumption of oxygen: a mitochondrial-generated progression signal of advanced cancer. in Cell death & disease 2012
These observations suggest that miR-149-3p can promote cancer progression via coordinated inhibition of DAB2IP in tumor cells and in stromal cells.
our study reveals an elevated expression of DAB2IP which could be modulated via the parallel down-regulation of EZH2 and mir-363-3p.
High expression serum miR-1266 had lower overall survival rates than patients with miR-1266 low expression. MiR-1266 promoted cell viability, proliferation, migration and invasion by targeting DAB2IP. And miR-1266 could promote tumorigenesis in vivo. In conclusion, miR-1266 could be used as a new biomarker for diagnosis, prediction and treatment of cervical cancer in the future.
The risk allele (A; rs7025486) was significantly associated with premature coronary artery disease in Indian population
Our study shows that DAB2IP harbored frameshift mutations and intratumoral heterogeneity as well as expression loss in gastric and colorectal cancers
The results indicated significant down-regulation of DAB2IP transcript variant 1 in prostatic cancerous tissues compared to paired normal tissues
The role of miR-367 in the pathogenesis of osteosarcoma via DAB2IP expression is reported.
mutp53 augments insulin-induced AKT1 activation by binding and inhibiting the tumor suppressor DAB2IP (DAB2-interacting protein) in the cytoplasm
variants DAB2IP-rs7025486[A] and SORT1-rs599839[G] are associated with abdominal aortic aneurysm expansion.
Low expression of DAB2IP is associated with nasopharyngeal carcinoma.
These findings suggest that DAB2IP is a direct target of miRNA-556-3p, and endogenous miRNA-556-3p expression shows inverse correlation with simultaneous DAB2IP expression in bladder cancer (BC)tissues and cells. miRNA-556-3p functions as a tumor promoter in tumorigenesis and metastasis of BC by targeting DAB2IP
Low DAB2IP expression is associated with neoplasms.
Results identified PRRT2 and DAB2IP to be frequently mutated in all different cancer cell line types. Further analysis showed that both genes were also frequently mutated in colorectal and endometrial cancer patient samples.
Data suggest that DAB2IP CpG1 methylation is a practical and repeatable biomarker for renal cell carcinoma (ccRCC), which can provide prognostic value that complements the current staging system.
PROX1 overexpression in DAB2IP-deficient prostate cancer cells could enhance the accumulation of HIF1alpha protein by inhibiting ubiquitin pathway and then consequently induce an epithelial-mesenchymal transition response.
Study shows that up to 62% of luminal B cancers have lost expression of at least one of the DAB2IP and RASAL2 genes. However, the tumors that have lost both genes frequently present as advanced disease and are more likely to recur. Importantly, the report provide evidence that DAB2IP and RASAL2 can individually function as tumor suppressors in breast cancer.
The low expression of DAB2IP in bladder carcinoma cells was related to drug resistance.
Down-regulation of DAB2IP correlated negatively with hnRNPK and MMP2 expressions in CRC tissues. In conclusion, our study elucidates a novel mechanism of the DAB2IP/hnRNPK/MMP2 axis in the regulation of CRC invasion and metastasis, which may be a potential therapeutic target.
DAB2IP appears to be a new prognostic/predictive marker for metastatic renal cell cancer (mRCC) patients, and its function provides a new insight into the molecular mechanisms of drug resistance to mTOR inhibitors, which also can be used to develop new strategies to overcome drug-resistant mRCC.
Along with the reduction of ovarian cancer-2/disabled homolog 2 (DOC-2/DAB2) interactive protein (DAB2IP) expression, EGR-1 gene was upregulated in FI-treated cells. On the other hand, downregulation of EGR-1 gene expression sensitized radioresistant cells to IR accompanied by DAB2IP overexpression and STAT3 inactivation. In addition, NF-kappaB inhibitor, BAY11-7082 enhanced resistant cells' radiosensitivity and chemos...
DAB2IP loss reprograms intracellular signal transduction and anti-apoptotic gene expression, which potentiates prostate cancer cell survival from androgen deprivation therapy-induced cell death.
Germ cell-specific or Sertoli cell-specific deletion of Aip1 gene each led to significant defects in germ cell migration after postnatal day 4 or 5, accompanied by elevated levels of actin filaments (F-actin) in the affected cells.
Cor1B, Cof1 and AIP1 work in concert through a temporally ordered pathway to induce highly efficient severing and disassembly of actin filaments.
results suggest that Dab2IP plays an important role in the migration and positioning of a subpopulation of later-born (layers II-IV) neurons, likely through the regulation of Rap1 and integrin signaling.
Our data reveal that AIP1, by inhibiting VEGFR2-dependent signaling in tumor niche, suppresses tumor EMT switch, tumor angiogenesis, and tumor premetastatic niche formation to limit tumor growth and metastasis.
AIP1 was elevated in the brain of AD Tg2576 mice. Abeta1-42 treatment induced the interaction of AIP1 and ASK1, which led to dissociation of ASK1 and 14-3-3.
site-specific methylation of mDab2ip gene during cerebellar development may play a role in inclusion of exon 5, resulting in a Dab2ip transcript variant that encodes a full pleckstrin homology (PH) domain.
Study showed that DAB2IP can be functionally inactivated by physical interaction with mutant p53 proteins with implications for the response of cancer cells to inflammatory cytokines.
DAB2IP is a unique intrinsic androgen receptor modulator in normal cells, and likely can be further developed into a therapeutic agent for rpostate cancer.
AIP1 knockouts have reduced retinal angiogenesis. Vascular endothelial cell (but not neuronal)-specific deletion of AIP1 causes similar defects. AIP1 via miR-1236 increases VEGFR-3 expression and binds it, enhancing endocytosis and stability.
Dab2IP plays an important role in dendrite development and regulates the number of synapses in the cerebellum.
Knock down of Dab2ip in neurons ex-vivo indicates that this protein is necessary for proper neurite development and for the expression of several major neuronal microtubule associated proteins
Loss of endothelial AIP1 in contributes to the exacerbated lesion expansion in the ApoE(-/-)AIP1(-/-) mice, revealing an important role of AIP1 in limiting inflammation, EC dysfunction, and atherosclerosis.
Both internalization and ASK1-interacting protein-1 association are required for TNFR2-dependent JNK and apoptotic signaling in endothelial cells.
AIP1 prevents graft arteriosclerosis by inhibiting interferon-gamma-dependent smooth muscle cell proliferation and intimal expansion.
Data define a role of DAB2 in fate determination of embryonic stem cells and suggests the presence of a DAB2-associated regulatory circuit in the control of mesoderm differentiation.
This study suggests that Dab2IP may function as a downstream effector in the Reelin signaling pathway that influences Ras signaling during brain development.
AIP1 is essential for transducing the IRE1-mediated endoplasmic reticulum stress response.
DAB2IP is a Ras (MIM 190020) GTPase-activating protein (GAP) that acts as a tumor suppressor. The DAB2IP gene is inactivated by methylation in prostate and breast cancers (Yano et al., 2005
DAB2 interacting protein
, ASK-interacting protein 1
, ASK1-interacting protein 1
, DAB2 interaction protein
, DAB2-interacting protein
, DOC-2/DAB-2 interactive protein
, DOC-2/DAB2 interactive protein
, disabled homolog 2-interacting protein
, nGAP-like protein
, apoptosis signal-regulating kinase 1-interacting protein 1
, disabled homolog 2 interacting protein
, DOC2/DAB2 interactive protein
, disabled 2 interacting protein long form