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Human Monoclonal ING1 Primary Antibody for ICC, IF - ABIN2668666
Boland, Olineck, Bonnefin, Vieyra, Parr, Riabowol: A panel of CAb antibodies recognize endogenous and ectopically expressed ING1 protein. in Hybridoma 2000
Show all 2 Pubmed References
ING1a induces these changes through strongly inhibiting endocytosis to block mitogen signaling by inducing the expression of intersectin 2, a key scaffolding protein of the endosomal pathway.
Over-expression of ING1 dramatically inhibited non-small cell lung cancer cells proliferation, migration and invasion.
The p37 controls cortical NuMA levels via the phosphatase PP1 and its regulatory subunit Repo-Man, but it acts independently of Galphai, the kinase Aurora A, and the phosphatase PP2A.
Nuclear entrapment of p33ING1b by inhibition of exportin-1 triggers apoptosis in head and neck squamous cell cancer cells.
Results from a study on gene expression variability markers in early-stage human embryos shows that ING1 is a putative marker for the 3-day, 8-cell embryo stage.
Our findings provide evidence for a novel crosstalk and a crossregulation between ING1 and ING2 in regulating androgen receptor-mediated transactivation and suggest that ING2 acts as a novel corepressor that inhibits AR signaling, prostate cancer cell growth, and migration.
ING1 regulates the nucleolar epigenome and rDNA transcription suggesting that regulation of protein synthesis might serve as the basis for ING1 function as a type II tumor suppressor.
a novel corepressor function of ING1b on various AR functions, thereby inhibiting prostate cancer cell growth.
ING1a acts as a novel link in the activation of the Rb pathway that can impose senescence in the absence of activating p53-mediated DNA damage signaling, and should prove useful in defining the molecular events contributing to Rb-induced senescence.
These data indicate that stromal ING1 expression can predict the survival of patients with luminal breast cancer
Overexpression of let-7b in gastric cancer can inhibit invasion and migration of gastric cancer cells through directly targeting the tumor metastasis-associated gene ING1.
Results show that ING1 expression is under-regulated in pancreatic duct adenocarcinoma (PDAC) and is a direct target of miR-371-5p involved in miR-371-5p inducing promotion of PDAC cells proliferation.
ING1b finely regulates the hypoxic response by triggering HIF1alpha proteasomal degradation.
ING1b sumoylation regulates the binding of ING1b to the ISG15 and DGCR8 promoters, consequently regulating ISG15 and DGCR8 transcription.
Our results identify a novel functional relationship between cytoplasmic p33ING1b and oral squamous cell carcinoma patient survival
Ing1b lacking cells showed decreased ability to repair the oxidized DNA.
ING1 translocates to the mitochondria of primary fibroblasts and established epithelial cell lines in response to apoptosis inducing stimuli, independent of the cellular p53 status.
ING1 acts at early stages of the DNA damage response activating a variety of repair mechanisms.
Src may play a major role in regulating ING1 levels during tumorigenesis in those cancers in which high levels of Src expression or activity are present.
Data identify a pathway by which ING1a induces senescence and indicate that altered endocytosis activates the Rb pathway, subsequently effecting a senescent phenotype.
ING1 knockdown leads to decreased expression of genes related to synaptic plasticity, including the regulatory subunit of calcineurin, Ppp3r1. In addition, ING1 binding at a site upstream of the transcription start site (TSS) of Ppp3r1 depends on yet another group of neuroepigenetic regulatory proteins, the Piwi-like family, which are also involved in DNA repair.
Taken together, our findings provide evidence for a novel crosstalk and a crossregulation between ING1 and ING2 in regulating androgen receptor-mediated transactivation and suggest that ING2 acts as a novel corepressor that inhibits AR signaling, prostate cancer cell growth, and migration.
ING1b is an important regulator of osteoblast differentiation and suppresses PPAR-beta/delta.
Increased melanoma formation and dissemination in TyrNRas mice deficient in the tumor suppressor Ing1.
Study reveals a novel connection between ING1 and a regulator of microRNA biogenesis and identifies new links between tumor suppressor proteins and the microRNA machinery.
Identification of the p33(ING1)-regulated genes that include cyclin B1 and proto-oncogene DEK by using cDNA microarray in a mouse mammary epithelial cell line NMuMG
Characterization of nuclear localization signal in mouse ING1 homolog protein.
p33ING1 expression induces features of cellular senescence through two silencing domains and interaction with Ras
the suggested role of ing1 as a candidate tumor suppressor gene involved in control of DNA damage response.
p37(Ing1) can negatively regulate cell growth and apoptosis in a p53-independent manner.
important role for the Ing1 locus in protection against oncogenic stress in vivo, both as a mediator of p53 activation and as a regulator of chromatin remodeling processes.
Analysis of marker gene expression in p37(Ing1b)/p53 null tumors indicates that the double-null mice develop both nongerminal center and germinal center B-cell-like DLBL.
A more sophisticated approach, using neural networks, permits prediction of interaction among three or more genes (p53, bax, and ING1).
This gene encodes a tumor suppressor protein that can induce cell growth arrest and apoptosis. The encoded protein is a nuclear protein that physically interacts with the tumor suppressor protein TP53 and is a component of the p53 signaling pathway. Reduced expression and rearrangement of this gene have been detected in various cancers. Multiple alternatively spliced transcript variants encoding distinct isoforms have been reported.
growth inhibitor ING1
, growth inhibitory protein ING1
, inhibitor of growth protein 1
, tumor suppressor ING1
, inhibitor of growth family, member 1