anti-Growth Arrest and DNA-Damage-Inducible, gamma Interacting Protein 1 (GADD45GIP1) Anticorps

Human Growth Arrest and DNA-Damage-Inducible, gamma Interacting Protein 1 (GADD45GIP1) interaction partners

1. NRF2 Ser40 phosphorylation was inhibited in Crif1-deficient bone marrow multipotent mesenchymal stromal cells even in the presence of three kinds of PKC agonists, suggesting that CRIF1 might co-activate PKC-delta to phosphorylate NRF2 Ser40.

2. strongly suggest that CRIF1 deficiency promotes endothelial cell inflammation by increasing VCAM-1 expression, elevating inflammatory cytokines levels, and activating the transcription factor NF-kappaB, all of which were inhibited by SIRT1 overexpression

3. Results demonstrate that knockdown of CRIF1 in HUVECs induces mitochondrial dysfunction and reduces SIRT1 expression along with decreased eNOS phosphorylation and increased eNOS acetylation, thereby promoting endothelial dysfunction. These findings indicate that CRIF1 plays an important role in maintaining mitochondrial and endothelial function through its effects on the SIRT1-eNOS pathway.

4. SNF5 is indispensable for CRIF1-enhanced p53 activity and its function in the suppression of cell cycle arrest in human cancer cells.

5. Study shows that Lck interacts with CRIF1 in the mitochondria and negatively regulates CRIF1-mediated translation of mitochondrion-encoded proteins.

6. our results support a novel function of nuclear Lck in promoting human leukemic T cell survival through interaction with a tumor suppressor, CRIF1

7. Crif1 is an indispensable regulator of PKAalpha cat that modulates the PKA/CREB signaling pathway to promote adipogenic differentiation of bone marrow mesenchymal stem cells after irradiation

8. The results identify the ROS-Sp1-Crif1 pathway to be a new mechanism underlying Abeta-induced mitochondrial dysfunction and suggest that ROS-mediated downregulation of Crif1 is a crucial event in AD pathology.

9. CRIF1 knockdown partially induces endothelial activation via increased ROS production and phosphorylation of p66shc

10. CRIF1 may play a regulatory role in the BM microenvironment-induced leukemia cell cycle arrest possibly through interacting with CDK2 and acting as a cyclin-dependent kinase inhibitor.

11. CKbetaBP2/CRIF1 is expressed with STAT3 in prostate cancer where STAT3 may help to offset the AR repressor effect of CKbetaBP2/CRIF1.

12. results indicated cell cycle arrest of Jurkat cells in the G0/G1 phase to be induced by primary cultured leukemic BMSCs associated with increased expression of CRIF1 by leukemic cells

13. CRIF1, unlike KEAP1 (which only interacts with N-terminal region of NRF2), physically interacts with both N- and C-terminal regions of NRF2 and promotes NRF2 ubiquitination and subsequent proteasome-mediated NRF2 protein degradation

14. results suggest that CRIF1 is a novel nuclear protein that interacts with Gadd45 and may play a role in negative regulation of cell cycle progression and cell growth

15. Phosphorylation of serine-221 in CKBBP2/CRIF1 promotes proliferation of green monkey COS7 cells.

16. NAC-1 contributes to tumor growth and survival by at least inhibiting Gadd45GIP1 expression, which has a tumor suppressor effect in cancer cells.

17. Results suggest that CRIF1 acts as an AR corepressor and may play an important role in the regulation of AR-positive growth of prostate cancer.

Mouse (Murine) Growth Arrest and DNA-Damage-Inducible, gamma Interacting Protein 1 (GADD45GIP1) interaction partners

1. Crif1(beta-/-) mouse is a useful model for the study of beta cell failure caused by mitochondrial OxPhos dysfunction.

2. The results identify the ROS-Sp1-Crif1 pathway to be a new mechanism underlying Abeta-induced mitochondrial dysfunction and suggest that ROS-mediated downregulation of Crif1 is a crucial event in AD pathology.

3. CRIF1 knockdown partially induces endothelial activation via increased ROS production and phosphorylation of p66shc

4. Study showed that loss of Crif1 impairs mitochondrial oxidative phosphorylation and adipocyte differentiation in vitro and in vivo.

5. Crif1 plays a critical role in the maintenance of both mitochondrial structure and respiration in cardiac muscles.

6. Although adipose-specific Crif1-haploinsufficient mice showed normal growth and development, they became insulin-resistant.

7. CRIF1 is essential for the synthesis and insertion of oxidative phosphorylation polypeptides in the mammalian mitochondrial membrane.

8. Results reveal that Crif1 is a novel and essential transcriptional coactivator of Elf3 for the terminal differentiation of absorptive enterocytes.

9. Crif1 is a novel and essential transcriptional coactivator of STAT3 that modulates its DNA binding ability.