Browse our anti-ABCC5 (ABCC5) Antibodies

Human ATP-Binding Cassette, Sub-Family C (CFTR/MRP), Member 5 (ABCC5) interaction partners

1. ABCC5 polymorphisms may explain partially the interpatient variability in doxorubicin disposition.

2. This study is the first to identify the roles of FOXM1 in drug efflux and paclitaxel resistance by regulating the gene transcription of abcc5, one of the ABC transporters. Small molecular inhibitors of FOXM1 or ABCC5 have the potential to overcome paclitaxel chemoresistance in nasopharyngeal carcinoma (NPC)patients.

3. These findings enrich the allelic spectrum of ABCC5 in PACG. We identified no tagging SNP responsible for the association of the whole region.

4. Survivors of childhood acute lymphoblastic leukemia treated with doxorubicin with the ABCC5 TT-1629 genotype had an average of 8-12% reduction of ventricular ejection and shortening fractions.

5. our work indicated that decreased SLC34A2 expression sensitized BCSCs to doxorubicin via SLC34A2-Bmi1-ABCC5 signaling and shed new light on understanding the mechanism of chemoresistance in BCSCs. This study not only bridges the missing link between stem cell-related transcription factor (Bmi1) and ABC transporter (ABCC5) but also contributes to development of potential therapeutics against breast cancer.

6. Deletions of ABCC5 predict good tumor response to neoadjuvant chemotherapy in breast cancer.

7. genetic association study in population in Mexico: Data suggest SNPs in ABCC5 (3933+313T>C) are not associated with adverse reactions to methotrexate; they protect against myelosuppression in pediatric patients with ALL (acute lymphoblastic leukemia).

8. We identified several genes (FasL, MSH2, ABCC5, CASP3, and CYP3A4)that showed association with PFS in patients with osteosarcoma. These pharmacogenetic risk factors might be useful to predict treatment outcome

9. ABCC5 is a general glutamate conjugate and analog transporter that affects the disposition of endogenous metabolites, toxins, and drugs.

10. The present study investigated the time course and dose dependency of the induction of three efflux proteins, P-gp, MRP1 and MRP5, in response to gemcitabine exposure in Capan-2 pancreatic cancer cell line at transcriptional and translational levels.

11. cCMP is a substrate for MRP5

12. The blockade of ABC transporter MRP5 could help to improve drug effectiveness, reduce tumour growth and prevent recurrence in glioblastoma multiforme.

13. To identify substrates of orphan transporter ATP-binding cassette subfamily C member 5 (ABCC5), identified a class of metabolites, N-lactoyl-amino acids, and found that a protease, cytosolic nonspecific dipeptidase 2 (CNDP2), catalyzes their formation.

14. ABCC5 transporter is a novel type 2 diabetes susceptibility gene in European and African American populations.

15. ABCC5 functions as a mediator of breast cancer skeletal metastasis. ABCC5 expression in breast cancer cells is important for efficient osteoclast-mediated bone resorption.

16. This locus was associated with an increase in risk of PACG in a separate case-control study of 4,276 primary angle closure glaucoma cases and 18,801 controls (per-allele OR = 1.13 [95% CI: 1.06-1.22], P = 0.00046).

17. Further research is needed to clarify whether MRP5 is indicative of malignant pathological features in meningiomas and whether possible therapeutic implications exist

18. PDE5 is highly expressed and increases ( approximately 130%) during growth whereas ABCC5 exhibited low to moderate expression, with a moderate increase ( approximately 40%) during growth

19. The present results imply that MRP5 index may hold a prognostic role in patients with glioblastoma multiforme

20. Findings show that the gene expression of ATP-dependent efflux transporters MRP1, -3, -4, -5, and p-gp fluctuated during stem cell-derived retinal pigment epithelial cells (hESC-RPE) maturation.

Mouse (Murine) ATP-Binding Cassette, Sub-Family C (CFTR/MRP), Member 5 (ABCC5) interaction partners

1. ABCC5 is a general glutamate conjugate and analog transporter that affects the disposition of endogenous metabolites, toxins, and drugs.

2. Deficiency of MKP5 resulted in increased inflammatory activation in macrophages. These findings thus demonstrate that MKP5 critically controls inflammation in white adipose tissue and the development of metabolic disorders

3. Reduced cGMP export as a consequence of decreased MRP5 expression can attenuate heart failure in sepsis.

Rabbit ATP-Binding Cassette, Sub-Family C (CFTR/MRP), Member 5 (ABCC5) interaction partners

1. Higher expression of MRP5 in muscle cells from fundus correlates with tonic phenotype of muscle.