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IASPP is one of the most evolutionarily conserved inhibitors of p53 (TP53; MIM 191170), whereas ASPP1 (MIM 606455) and ASPP2 (MIM 602143) are activators of p53..
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Cow (Bovine) Polyclonal PPP1R13L Primary Antibody for IHC, WB - ABIN2777612
Tomoda, Takahashi, Hibi, Asamitsu, Ishida, Kondo, Fujii, Okamoto: Molecular docking analysis of the protein-protein interaction between RelA-associated inhibitor and tumor suppressor protein p53 and its inhibitory effect on p53 action. in Cancer science 2008
Dog (Canine) Polyclonal PPP1R13L Primary Antibody for ELISA, WB - ABIN2474107
Zhang, Diao, Rao, Xing, Liu, Liao, Wang, Wang: Identification of a novel isoform of iASPP and its interaction with p53. in Journal of molecular biology 2007
miR (show MLXIP Antibodies)-182 plays an aggressive role in the cerebral ischemia injury, and this is associated with inhibited iASPP expression.
iASPP expression may act as a predictive marker of prostate cancer progression.
These data demonstrate that by interacting with desmoplakin (show DSP Antibodies) and desmin (show DES Antibodies), iASPP is an important regulator of desmosomal function both in vitro and in vivo.
p53 (show TP53 Antibodies)-mediated neuronal cell death after stroke can be nontranscriptionally regulated by a novel mechanism involving suppression of endogenous cell death inhibitors by miR (show MLXIP Antibodies)-124.
PPP1R13L has an essential role in embryonic eyelid closure as well in development of meibomian glands and the anterior segment of the eye
These data showed iASPP to be a key regulator of epithelial homeostasis in skin.
Inhibitor of apoptosis-stimulating protein of p53 (iASPP) prevents senescence and is required for epithelial stratification.
Mice with mutation in Nkip1 (Ppp1r13l) represent a potentially important model for the analysis of the role of inflammatory processes in heart disease.
Studies revealed that overexpression of PPP1R13L causes faster p53 (show TP53 Antibodies) degradation, a likely explanation for the depletion of p53 (show TP53 Antibodies).
Data showed that iASPP could promote tumor growth by increasing autophagic flux, and iASPP could serve as a poor prognostic factor and a potential therapeutic target in lung cancer.
Sertad1 (show SERTAD1 Antibodies) could antagonize iASPP function by hindering its entrance into nuclei to interact with P53 (show TP53 Antibodies) in leukemic cells when iASPP was in the stage of overproduction.
The interactive modulation among miR (show MLXIP Antibodies)-124 and iASPP in p53 (show TP53 Antibodies)-mutant or -deleted cells may serve as a crucial pathway, which mediates therapy resistance when p53 (show TP53 Antibodies) is mutated or deleted, in the process of photodynamic therapy treatment of Colorectal cancer.
These findings indicated that XIST may regulate the tumor growth and metastasis via miR (show MLXIP Antibodies)-140-dependent iASPP regulation. Taken together, our data indicated that XIST may be an oncogenic lncRNA that promotes the proliferation and metastasis of lung cancer through the regulation of miR (show MLXIP Antibodies)-140 and could be regarded as a therapeutic target in human lung cancer.
FHL2 (show FHL2 Antibodies) and iASPP interacted with each other and co-localized in both nucleus and cytoplasm. Either FHL2 (show FHL2 Antibodies) or iASPP silenced could reduce cell proliferation, induce cell cycle arrest at G0/G1 phase, and increase cell apoptosis.
the restoration of miR (show MLXIP Antibodies)-124 reduces iASPP expression and leads to p53 (show TP53 Antibodies)-dependent tumor suppression, suggesting a therapeutic strategy to treat iASPP-associated cervical cancer.
miR (show MLXIP Antibodies)-124 regulates p63 (show RPE65 Antibodies) via iASPP, while p63 (show RPE65 Antibodies) targets miR (show MLXIP Antibodies)-155 via the modulation of STAT1 (show STAT1 Antibodies) expression in colorectal cancer.
TP73-AS1 inhibited the brain glioma growth and metastasis as a competing endogenous RNA (ceRNA) through miR (show MLXIP Antibodies)-124-dependent iASPP regulation.
findings revealed the detailed role of the miR (show MLXIP Antibodies)-184/iASPP axis in Central nervous system lymphoma (CNSL) and this axis might modulate the proliferation and invasion of CNSL via regulating the PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies) signaling pathway.
Data suggest that Keap1 (show KEAP1 Antibodies), rather than Nrf2 (show GABPA Antibodies), is critical for the recruitment of iASPP into the Keap1 (show KEAP1 Antibodies)-Nrf2 (show GABPA Antibodies) complex
Frameshift mutation in PPP1R13L causes Cardiomyopathy and woolly haircoat syndrome in Poll Hereford cattle.
Data suggest Greatwall (show MASTL Antibodies) kinase (Gwl (show MASTL Antibodies)) associates with protein phosphatase 1 (show PPP1CB Antibodies) (PP1), particularly PP1gamma subunit, which mediates dephosphorylation of Gwl (show MASTL Antibodies) Ser (show SIGLEC1 Antibodies)-883; consistent with mitotic activation of Gwl (show MASTL Antibodies), its association with PP1 is disrupted in mitotic cells; subunits PPP1R3B (show PPP1R3B Antibodies) and PPP1R13L associate with Gwl (show MASTL Antibodies); thus, PPP1R3B (show PPP1R3B Antibodies) appears to act as cell cycle regulator in oocytes that functions by governing Gwl (show MASTL Antibodies) dephosphorylation.
IASPP is one of the most evolutionarily conserved inhibitors of p53 (TP53\; MIM 191170), whereas ASPP1 (MIM 606455) and ASPP2 (MIM 602143) are activators of p53.
NFkB interacting protein 1
, NFkB-interacting protein 1
, PPP1R13B-like protein
, inhibitor of ASPP protein
, protein iASPP
, relA-associated inhibitor
, inhibitor of apoptosis stimulating protein of p53
, protein phosphatase 1, regulatory (inhibitor) subunit 13 like
, retinoic acid induced 4