Protein Phosphatase 1, Regulatory Subunit 13 Like (PPP1R13L) ELISA Kits

Mouse (Murine) Protein Phosphatase 1, Regulatory Subunit 13 Like (PPP1R13L) interaction partners

1. The identification of a cell autonomous role of iASPP deficiency in causing cardiocutaneous syndrome, impaired eyelid development and wound healing suggests that variants in the iASPP gene also may contribute to polygenic heart and skin diseases.

2. miR-182 plays an aggressive role in the cerebral ischemia injury, and this is associated with inhibited iASPP expression.

3. iASPP expression may act as a predictive marker of prostate cancer progression.

4. These data demonstrate that by interacting with desmoplakin and desmin, iASPP is an important regulator of desmosomal function both in vitro and in vivo.

5. p53-mediated neuronal cell death after stroke can be nontranscriptionally regulated by a novel mechanism involving suppression of endogenous cell death inhibitors by miR-124.

6. PPP1R13L has an essential role in embryonic eyelid closure as well in development of meibomian glands and the anterior segment of the eye

7. These data showed iASPP to be a key regulator of epithelial homeostasis in skin.

8. Inhibitor of apoptosis-stimulating protein of p53 (iASPP) prevents senescence and is required for epithelial stratification.

9. Mice with mutation in Nkip1 (Ppp1r13l) represent a potentially important model for the analysis of the role of inflammatory processes in heart disease.

10. Studies revealed that overexpression of PPP1R13L causes faster p53 degradation, a likely explanation for the depletion of p53.

Human Protein Phosphatase 1, Regulatory Subunit 13 Like (PPP1R13L) interaction partners

1. Acute myeloid leukemia patients with high expressions of FHL2 and iASPP had shorter event-free survival (EFS) and overall survival (OS) than patients with low expressions.

2. High iASPP expression is associated with chemoresistant ovarian clear cell carcinoma.

3. Haplotypes consisting of PPP1R13L rs1970764 and ATM rs11212592 may be associated with lung cancer. Haplotypes consisting of PPP1R13L, CD3EAP and GLTSCR1 SNPs on Chr19q13.3 may associate with lung cancer risk in the Chinese population.

4. The expression of CD3EAP exon 1 was demonstrated to be significantly associated with PPP1R13L exon 1, while CD3EAP exon 3 was significantly associated with ERCC1 exon 11 in normal and non-small cell lung cancer (NSCLC) tissues. It was observed that short transcripts of ERCC1, CD3EAP and PPP1R13L are co-expressed in A549 NSCLC cell line.

5. Increased expression of miR-150 suppressed viability, proliferation, migration and invasion of SW480 cells. Furthermore, iASPP was a direct target of miR-150 and played a key role in its anti-colorectal cancer (CRC)function. miR-150 may be a promising predictor of prognosis in CRC patients.

6. IASPP knockdown suppressed cell viability and DNA synthesis capacity; the effect of miR-340 inhibition was partially attenuated by iASPP inhibition.

7. The expression of iASPP was higher in highgrade astrocytic gliomas compared with lowgrade astrocytic gliomas.

8. 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.

9. Sertad1 could antagonize iASPP function by hindering its entrance into nuclei to interact with P53 in leukemic cells when iASPP was in the stage of overproduction.

10. The interactive modulation among miR-124 and iASPP in p53-mutant or -deleted cells may serve as a crucial pathway, which mediates therapy resistance when p53 is mutated or deleted, in the process of photodynamic therapy treatment of Colorectal cancer.

11. These findings indicated that XIST may regulate the tumor growth and metastasis via miR-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-140 and could be regarded as a therapeutic target in human lung cancer.

12. FHL2 and iASPP interacted with each other and co-localized in both nucleus and cytoplasm. Either FHL2 or iASPP silenced could reduce cell proliferation, induce cell cycle arrest at G0/G1 phase, and increase cell apoptosis.

13. the restoration of miR-124 reduces iASPP expression and leads to p53-dependent tumor suppression, suggesting a therapeutic strategy to treat iASPP-associated cervical cancer.

14. miR-124 regulates p63 via iASPP, while p63 targets miR-155 via the modulation of STAT1 expression in colorectal cancer.

15. TP73-AS1 inhibited the brain glioma growth and metastasis as a competing endogenous RNA (ceRNA) through miR-124-dependent iASPP regulation.

16. findings revealed the detailed role of the miR-184/iASPP axis in Central nervous system lymphoma (CNSL) and this axis might modulate the proliferation and invasion of CNSL via regulating the PI3K/Akt signaling pathway.

17. Data suggest that Keap1, rather than Nrf2, is critical for the recruitment of iASPP into the Keap1-Nrf2 complex

18. Three htSNPs (haplotype-tagging single nucleotide polymorphism) (rs7354, rs14384, and rs3783501) covering 95% of the common haplotype diversity in 19p13.3-GADD45B and interaction of 19p13.3-GADD45B and 19q13.3-PPP1R13L and 19q13.3-CD3EAP variants and smoking-duration were explored in lung cancer risk Chinese.

19. We describe the identification of a maternally inherited frameshift mutation in RAI1, causative for SMS. This is the first report about transmission of SMS from an affected parent to an offspring.

20. These results determined PPP1R13L as the gene underlying a novel autosomal-recessive cardio-cutaneous syndrome in humans and strongly suggest that the fatal dilated cardiomyopathy during infancy is a consequence of failure to regulate transcriptional pathways necessary for tuning cardiac threshold response to common inflammatory stressors.

Cow (Bovine) Protein Phosphatase 1, Regulatory Subunit 13 Like (PPP1R13L) interaction partners

1. Frameshift mutation in PPP1R13L causes Cardiomyopathy and woolly haircoat syndrome in Poll Hereford cattle.

Xenopus laevis Protein Phosphatase 1, Regulatory Subunit 13 Like (PPP1R13L) interaction partners

1. Data suggest Greatwall kinase (Gwl) associates with protein phosphatase 1 (PP1), particularly PP1gamma subunit, which mediates dephosphorylation of Gwl Ser-883; consistent with mitotic activation of Gwl, its association with PP1 is disrupted in mitotic cells; subunits PPP1R3B and PPP1R13L associate with Gwl; thus, PPP1R3B appears to act as cell cycle regulator in oocytes that functions by governing Gwl dephosphorylation.