Cereblon (CRBN) ELISA Kits

Human Cereblon (CRBN) interaction partners

1. This work suggests that the binding domain in CRBN is a critical factor which influences the regulation of immunomodulatory drugs on the ubiquitination and stability of these CRBN-interacting partners.

2. SALL4 has a role mediating teratogenicity as a thalidomide-dependent cereblon substrate

3. the ubiquitin-conjugating enzymes UBE2G1 and UBE2D3 cooperatively promote the K48-linked polyubiquitination of CRL4(CRBN) neomorphic substrates

4. insight paves the way for studies of CRBN-dependent proteasome-targeting molecules in nonprimate models and provides a new understanding of CRBN's substrate-recruiting function

5. Cereblon suppresses the formation of pathogenic protein aggregates in a p62-dependent manner.

6. mitochondrially expressed CRBN exhibited protease activity, and was induced by oxidative stress.

7. we identify Rabex-5 as a Immunomodulatory drugs (IMiDs) target molecule that functions to restrain TLR activated auto-immune promoting pathways. We propose that release of Rabex-5 from complex with Cereblon enables the suppression of immune responses, contributing to the antiinflammatory properties of IMiDs.

8. We sequenced CRBN-thalidomide binding region in 38 thalidomide embryopathy individuals and 136 Brazilians without congenital anomalies, and performed in silico analyses. Eight variants were identified, seven intronic and one in 3'UTR.

9. These findings thus contribute to a growing list of ID disorders caused by CRBN mutations, broaden the spectrum of phenotypes attributable to Autosomal-recessive non-syndromic intellectual disability (ARNS-ID)and provide new insight into genotype-phenotype correlations between CRBN mutations and the aetiology of ARNS-ID.

10. CRBN expression is of prognostic value in MM patients ineligible for ASCT treated with thalidomide as an immunomodulatory drug. With low expression indicating a possible suboptimal treatment outcome, measurement of CRBN expression might serve as additional prognostic tool in the personalized treatment approach.

11. Plasmablast differentiation, whether induced by BAFF or CD40L, is prevented by modulation of CRBN activity with CC-220, which induces degradation of the B cell differentiation factors Aiolos and Ikaros. Downregulation of these B cell differentiation processes by CC-220 modulation of CRBN provides a new therapeutic approach to treating B cell-mediated pathology in SLE.

12. High CRBN expression is associated with multiple myeloma.

13. CRBN negatively regulates TLR4 signaling via attenuation of TRAF6 and TAB2 ubiquitination.

14. Compared with newly diagnosed multiple myeloma, an increased prevalence of mutations in the Ras pathway genes KRAS, NRAS, and/or BRAF (72%), as well as TP53 (26%), CRBN (12%), and CRBN pathway genes (10%) was observed.

15. results suggest that CRBN binds to Ikaros via its N-terminal region and regulates transcriptional activities of Ikaros and its downstream target, enkephalin

16. dual assay demonstrated superior Cereblon IHC measurement in MM samples compared with the single IHC assay using a published commercial rabbit polyclonal Cereblon antibody and could be used to explore the potential utility of Cereblon as a biomarker in the clinic

17. IRF4 and CRBN polymorphisms affect risk and response to treatment in multiple myeloma

18. overview of the current understanding of mechanism of action of Immunomodulatory drugs via CRBN and prospects for the development of new drugs that degrade protein of interest.

19. 45.2 of multiple myeloma patients were CRBN(+). Among patients treated with thalidomide-based regimens, CRBN(+) patients showed a better treatment response than did CRBN-negative patients. There was no significant difference in survival outcomes between thalidomide- and bortezomib-based regimens in CRBN(+) patients.

20. These results support the notion that the cereblon binding partner AGO2 plays an important role in regulating MM cell growth and survival and AGO2 could be considered as a novel drug target for overcoming IMiD resistance in MM cells.

Mouse (Murine) Cereblon (CRBN) interaction partners

1. Crbn KO animals showed cognitive deficits caused by enhanced BK channel activity and reduced presynaptic glutamate release.

2. We show that Crbn is robustly expressed in the mouse hippocampus and Crbn(KO) mice exhibit hyperphosphorylated levels of AMPKalpha

3. dBET1 stimulates CRBN's E3 ubiquitin-conjugating function and degrades BRD4 in both mouse and human cells.

4. Cereblon suppresses the formation of pathogenic protein aggregates in a p62-dependent manner.

5. Collectively, our data suggested that CRBN is a potential treatment option against diabetes-induced osteolytic bone disease.

6. Data show that cereblon (CRBN) limits CD4(+) T-cell activation via epigenetic regulation of Kv1.3 potassium channel (Kv1.3) expression.

7. CRBN negatively regulates TLR4 signaling via attenuation of TRAF6 and TAB2 ubiquitination.

8. CRBN is involved in the activation of PERK and the Ire1 pathway of the unfolded protein response.CRBN plays a role in cellular stress signaling, including the unfolded protein response, by controlling the activity of AMPK.

9. results of this study suggest a plausible mechanism for CRBN involvement in higher brain function in humans, and they may help explain how a specific mutation in CRBN can affect the cognitive ability of patients

10. Found significantly smaller infarct sizes and less fibrosis in the hearts of CRBN KO mice than in those of WT mice. Apoptosis was also significantly reduced in the KO mice compared with that in WT mice.

11. findings suggest that crbn-/- mice exhibit selective HPC-dependent deficits in associative learning.

12. CRBN directly interacts with the alpha1 subunit of AMP-activated protein kinase (AMPK alpha1) and inhibits the activation of AMPK activation.

13. These results imply that Nrf2 stimulates CRBN gene transcription under hypoxia-reoxygenation conditions in neuronal cells.