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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 (show HNRNPK Proteins) and MMP2 (show MMP2 Proteins) expressions in CRC (show CALR Proteins) tissues. In conclusion, our study elucidates a novel mechanism of the DAB2IP/hnRNPK (show HNRNPK Proteins)/MMP2 (show MMP2 Proteins) axis in the regulation of CRC (show CALR Proteins) 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 (show FRAP1 Proteins) 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 (show DAB2 Proteins)/DAB2) interactive protein (DAB2IP) expression, EGR-1 (show EGR1 Proteins) gene was upregulated in FI-treated cells. On the other hand, downregulation of EGR-1 (show EGR1 Proteins) gene expression sensitized radioresistant cells to IR accompanied by DAB2IP overexpression and STAT3 (show STAT3 Proteins) inactivation. In addition, NF-kappaB (show NFKB1 Proteins) inhibitor, BAY11-7082 enhanced resistant cells' radiosensitivity and chemos...
Our findings demonstrate a novel function of DAB2IP in the maintenance of KT-MT structure and SAC (show ADCY10 Proteins) regulation during mitosis which is essential for chromosomal stability.
DAB2IP may be involved in forming acquired radioresistance in PC3 (show PCSK1 Proteins) cells. DAB2IP-deficient cells are resistant to low and high-LET radiation using different mechanisms. DAB2IP-deficient cells are resistant to both gamma-rays and alpha-particles.
our data provided evidence to verify that miR (show MLXIP Proteins)-92b was able to directly target DAB2IP, a well-known tumor suppressor, and inhibit epithelialmesenchymal transition of bladder cancer cells
DAB2IP protein levels are higher in bladder cancer than in upper tract urothelial carcinoma and in superficial bladder cancer
Infiltrating T cells regulate ERbeta (show ESR2 Proteins)/DAB2IP signals in renal cell carcinoma (show MOK Proteins).
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 (show PDCD6IP Proteins), by inhibiting VEGFR2 (show KDR Proteins)-dependent signaling in tumor niche, suppresses tumor EMT (show ITK Proteins) switch, tumor angiogenesis, and tumor premetastatic niche formation to limit tumor growth and metastasis.
AIP1 (show PDCD6IP Proteins) was elevated in the brain of AD Tg2576 mice. Abeta1-42 treatment induced the interaction of AIP1 (show PDCD6IP Proteins) and ASK1 (show MAP3K5 Proteins), which led to dissociation of ASK1 (show MAP3K5 Proteins) and 14-3-3 (show YWHAQ Proteins).
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 (show PLEK Proteins) homology (PH) domain.
Study showed that DAB2IP can be functionally inactivated by physical interaction with mutant p53 (show TP53 Proteins) proteins with implications for the response of cancer cells to inflammatory cytokines.
DAB2IP is a unique intrinsic androgen receptor (show AR Proteins) modulator in normal cells, and likely can be further developed into a therapeutic agent for rpostate cancer.
AIP1 (show PDCD6IP Proteins) knockouts have reduced retinal angiogenesis. Vascular endothelial cell (but not neuronal)-specific deletion of AIP1 (show PDCD6IP Proteins) causes similar defects. AIP1 (show PDCD6IP Proteins) via miR (show MLXIP Proteins)-1236 increases VEGFR-3 (show FLT4 Proteins) expression and binds it, enhancing endocytosis and stability.
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