Browse our Prohibitin 2 Proteins (PHB2)

Human Prohibitin 2 (PHB2) interaction partners

1. High PHB2 expression is associated with high ribosomal RNA transcription and facilitation of cell proliferation in rhabdomyosarcoma.

2. the present study suggested that PHB2 may promote Prostate cancer cell migration by inhibiting the expression of AKT2. These results provide information regarding the role of PHB2 in Prostate cancer migration and malignancy

3. Taken together, the results indicate that PHB2 plays a central role in p21 upregulation following GGCT knockdown and as such may promote deregulated proliferation of cancer cells by suppressing p21.

4. analysis of LGALS3, PHB2, MUC1, and GK2 expression with CA15-3 in early-stage breast cancer

5. Fluorizoline bind to prohibitin, inducing mitochondrial apoptotic pathway through NOXA and BIM upregulation.

6. REA modulates cross talk among multiple cell types in the uterine tissue and host background, serving as a brake on the estradiol-ER axis and restraining multiple aspects that contribute to the pathologic progression of endometriosis.

7. BIG3 may block the KPNAs (KPNA1, KPNA5, and KPNA6) binding region(s) of PHB2.

8. results show that PHB2 binds to the ligand binding domain of ERalpha with a conformational change in the helix 12 of ERalpha

9. Functional analysis of selected regulated proteins revealed that knockdown of HNRPD, PHB2 and UB2V2 can increase HCMV replication, while knockdown of A4 and KSRP resulted in decreased HCMV replication.

10. These results demonstrate that estradiol upregulates REA expression and recruits REA via ERalpha to the EREs on the RORgammaT promoter region, thus inhibiting RORgammaT expression and Th17 differentiation.

11. BIG3 (ARFGEF3) is predicted to interact with its partner PHB2 through an ARM-type alpha-helical structure.

12. Data indicate that the up-regulated expression of prohibitin promoted acute promyelocytic leukemia cell line NB4-R1 cell apoptosis.

13. PHB2 in hepatocellular carcinoma supports the development and progression of hepatocellular malignancy.

14. Prohibitin 2 acts as a nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells

15. BIG3(WRD5)-PHB2 interaction is critical for the tamoxifen resistance of breast cancer cells; its targeting reverses the resistance.

16. prohibitin and prohibiton (PHB2) contribute to PIG3-mediated apoptosis by binding to the PIG3 promoter (TGYCC)15 motif

17. Data indicate that IGFBP-6 binds to prohibitin-2 on the cell membrane, and knockdown of the latter abrogates IGFBP-6-induced migration.

18. Data demonstrate that PHB2 is essential for metabolic activation of mitochondria and, as a consequence, for function and survival of beta-cells.

19. ASURA specifically binds to chromatin when Scc1 is associated with chromatin.

20. PHBs are localized on the human platelet membrane and are involved in PAR1-mediated platelet aggregation.

Mouse (Murine) Prohibitin 2 (PHB2) interaction partners

1. Fluorizoline bind to prohibitin, inducing mitochondrial apoptotic pathway through NOXA and BIM upregulation.

2. REA modulates cross talk among multiple cell types in the uterine tissue and host background, serving as a brake on the estradiol-ER axis and restraining multiple aspects that contribute to the pathologic progression of endometriosis.

3. CARL can suppress mitochondrial fission and apoptosis by targeting miR-539 and PHB2.

4. These results demonstrate that estradiol upregulates REA expression and recruits REA via ERalpha to the EREs on the RORgammaT promoter region, thus inhibiting RORgammaT expression and Th17 differentiation.

5. results suggest that PHB2 is a crucial mitochondrial regulator for homeostasis and lineage-specific differentiation of ES cells.

6. Loss of PHB2 impairs the stability of OPA1, affects mitochondrial ultrastructure, and induces the perinuclear clustering of mitochondria in hippocampal neurons

7. REA physiologically restrains endometrial stromal cell decidualization, controlling the timing and magnitude of decidualization to coordinate uterine differentiation with concurrent embryo development that is essential for implantation and fertility.

8. PHB1 and PHB2 are critical mediators in promoting 3T3-L1 adipocyte differentiation and may be the potential targets for obesity therapies

9. Optimal uterine development and functional activities require the normal gene dosage of REA, with partial or complete deletion resulting in hyperresponsiveness or underresponsiveness to hormone and subfertility or infertility, respectively.

10. Serine phosphorylation of PHB2 by CaMK IV relieves its inhibition on MEF2.

11. Our findings reveal that REA is essential for mammary gland development and has a gene dosage-dependent role in the regulation of stage-specific physiological functions of the mammary gland.

12. REA has a role as a mediator of transcriptional repression by nuclear hormone receptors via recruitment of histone deacetylases

13. REA is a significant modulator of estrogen responsiveness in vivo: it normally restrains estrogen actions, moderating ER stimulation and enhancing ER repression of E2-regulated genes.

14. REA is a physiological modulator of ER function in the mammary gland, and its correct gene dosage is required for maintenance of normal ER activity and normal mammary gland development.

15. Skp2 variant Skp2B interacts with the repressor of estrogen receptor activity (REA) and that overexpression of Skp2B leads to a reduction in REA levels.

16. Results demonstrate that the repressor of estrogen receptor activity (REA), a protein related to PHB, interacts with PHB, to form heteromers and enhance the protein stability of both corepressors.

17. Deletion of Klf9 up-regulated uterine Phb2 expression and increased PHB2 nuclear localization in epithelial cells.

18. REA operates as a negative feedback modulator of TRPM6 in the regulation of active Mg(2+) (re)absorption and provides new insight into the molecular mechanism of renal transepithelial Mg(2+) transport.