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analysis of LGALS3, PHB2, MUC1, and GK2 expression with CA15-3 in early-stage breast cancer
Fluorizoline bind to prohibitin (show PHB ELISA Kits), inducing mitochondrial apoptotic pathway through NOXA (show PMAIP1 ELISA Kits) and BIM (show BCL2L11 ELISA Kits) upregulation.
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.
BIG3 (show WDR5 ELISA Kits) may block the KPNAs (KPNA1 (show KPNA1 ELISA Kits), KPNA5 (show KPNA5 ELISA Kits), and KPNA6 (show KPNA6 ELISA Kits)) binding region(s) of PHB2.
results show that PHB2 binds to the ligand binding domain of ERalpha (show ESR1 ELISA Kits) with a conformational change in the helix 12 of ERalpha (show ESR1 ELISA Kits)
Functional analysis of selected regulated proteins revealed that knockdown of HNRPD (show HNRNPD ELISA Kits), PHB2 and UB2V2 (show UBE2V2 ELISA Kits) can increase HCMV replication, while knockdown of A4 and KSRP (show KHSRP ELISA Kits) resulted in decreased HCMV replication.
These results demonstrate that estradiol upregulates REA expression and recruits REA via ERalpha (show ESR1 ELISA Kits) to the EREs on the RORgammaT promoter region, thus inhibiting RORgammaT expression and Th17 differentiation.
BIG3 (ARFGEF3) is predicted to interact with its partner PHB2 through an ARM-type alpha-helical structure.
Data indicate that the up-regulated expression of prohibitin (show PHB ELISA Kits) promoted acute promyelocytic leukemia (show PML ELISA Kits) cell line NB4-R1 cell apoptosis.
PHB2 in hepatocellular carcinoma supports the development and progression of hepatocellular malignancy.
CARL can suppress mitochondrial fission and apoptosis by targeting miR (show MLXIP ELISA Kits)-539 and PHB2.
results suggest that PHB2 is a crucial mitochondrial regulator for homeostasis and lineage-specific differentiation of ES cells.
Loss of PHB2 impairs the stability of OPA1 (show MED12 ELISA Kits), affects mitochondrial ultrastructure, and induces the perinuclear clustering of mitochondria in hippocampal neurons
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.
PHB1 (show PHB ELISA Kits) and PHB2 are critical mediators in promoting 3T3-L1 adipocyte differentiation and may be the potential targets for obesity therapies
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.
Serine phosphorylation of PHB2 by CaMK IV (show CAMK4 ELISA Kits) relieves its inhibition on MEF2 (show MEF2C ELISA Kits).
Acts as a mediator of transcriptional repression by nuclear hormone receptors via recruitment of histone deacetylases. Functions as an estrogen receptor (ER)-selective coregulator that potentiates the inhibitory activities of antiestrogens and represses the activity of estrogens. Competes with NCOA1 for modulation of ER transcriptional activity. Probably involved in regulating mitochondrial respiration activity and in aging (By similarity).
B-cell receptor-associated protein 37
, prohibitin 2
, B-cell associated protein
, B-cell receptor-associated protein BAP37
, repressor of estrogen receptor activity
, B-cell receptor associated protein 37