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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.[supplied by OMIM, Mar 2008].. Additionally we are shipping Protein Phosphatase 1, Regulatory Subunit 13 Like Antibodies (71) and Protein Phosphatase 1, Regulatory Subunit 13 Like Kits (4) and many more products for this protein.
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miR (show MLXIP Proteins)-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 and desmin (show DES Proteins), iASPP is an important regulator of desmosomal function both in vitro and in vivo.
p53 (show TP53 Proteins)-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 Proteins)-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 Proteins) degradation, a likely explanation for the depletion of p53 (show TP53 Proteins).
Increased expression of miR (show MLXIP Proteins)-150 suppressed viability, proliferation, migration and invasion of SW480 cells. Furthermore, iASPP was a direct target of miR (show MLXIP Proteins)-150 and played a key role in its anti-colorectal cancer (CRC (show CALR Proteins))function. miR (show MLXIP Proteins)-150 may be a promising predictor of prognosis in CRC (show CALR Proteins) patients.
IASPP knockdown suppressed cell viability and DNA synthesis capacity; the effect of miR (show MLXIP Proteins)-340 inhibition was partially attenuated by iASPP inhibition.
The expression of iASPP was higher in highgrade astrocytic gliomas compared with lowgrade astrocytic gliomas.
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 Proteins) could antagonize iASPP function by hindering its entrance into nuclei to interact with P53 (show TP53 Proteins) in leukemic cells when iASPP was in the stage of overproduction.
The interactive modulation among miR (show MLXIP Proteins)-124 and iASPP in p53 (show TP53 Proteins)-mutant or -deleted cells may serve as a crucial pathway, which mediates therapy resistance when p53 (show TP53 Proteins) 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 Proteins)-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 Proteins)-140 and could be regarded as a therapeutic target in human lung cancer.
FHL2 (show FHL2 Proteins) and iASPP interacted with each other and co-localized in both nucleus and cytoplasm. Either FHL2 (show FHL2 Proteins) 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 Proteins)-124 reduces iASPP expression and leads to p53 (show TP53 Proteins)-dependent tumor suppression, suggesting a therapeutic strategy to treat iASPP-associated cervical cancer.
miR (show MLXIP Proteins)-124 regulates p63 (show RPE65 Proteins) via iASPP, while p63 (show RPE65 Proteins) targets miR (show MLXIP Proteins)-155 via the modulation of STAT1 (show STAT1 Proteins) expression in colorectal cancer.
Frameshift mutation in PPP1R13L causes Cardiomyopathy and woolly haircoat syndrome in Poll Hereford cattle.
Data suggest Greatwall (show MASTL Proteins) kinase (Gwl (show MASTL Proteins)) associates with protein phosphatase 1 (show PPP1CB Proteins) (PP1), particularly PP1gamma subunit, which mediates dephosphorylation of Gwl (show MASTL Proteins) Ser (show SIGLEC1 Proteins)-883; consistent with mitotic activation of Gwl (show MASTL Proteins), its association with PP1 is disrupted in mitotic cells; subunits PPP1R3B (show PPP1R3B Proteins) and PPP1R13L associate with Gwl (show MASTL Proteins); thus, PPP1R3B (show PPP1R3B Proteins) appears to act as cell cycle regulator in oocytes that functions by governing Gwl (show MASTL Proteins) 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