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BI-1 affects cell death-associated components localized in sphingolipid-enriched microdomains of the plasma membrane.
AtBI-1 contributes to synthesis of sphingolipids during cold stress by interacting with AtSLD1, AtFAH1, AtSBH2 and AtADS2.
Arabidopsis thaliana BI-1-interacting proteins were identified.
The role of AtBI1 over-expression in delaying Methyl jasmonate-induced leaf senescence by suppressing the [Ca(2 (show CA2 ELISA Kits)+)](cyt (show CYGB ELISA Kits))-dependent activation of MPK6 (show MAPK6 ELISA Kits), thus providing a new insight into the function and mechanism of AtBI1 in plant senescence.
Overexpression of AtBI-1 increases the amount of 2-hydroxy fatty acids.
BAX INHIBITOR 1 is an attenuator for cell death progression triggered by both biotic and abiotic types of cell death signals in Arabidopsis.
The expression of AtBI-1, which suppresses Bax (show BAX ELISA Kits)-induced cell death, in the tapetum at the tetrad stage inhibits tapetum degeneration and subsequently results in pollen abortion, while activation of AtBI-1 at the later stage does not.
A study evaluating the effect of AtBI-1 on calcium homeostasis is reported.
BI-1 requires normal electron transport activity to suppress cell death in yeast
Results indicate that the loss of calmodulin binding reduces the cell death suppressor activity of Bax inhibitor-1 in planta.
BI-1 is overexpressed and promotes the progression and metastasis of non-small cell lung cancer
These results suggest that the TMBIM family has comparable functions in the maintenance of intracellular Ca(2 (show CA2 ELISA Kits)) homeostasis in a wide variety of tissues
Bax inhibitor-1 is likely a pH-sensitive calcium leak channel, not a H+/Ca2 (show CA2 ELISA Kits)+ exchanger.
BI-1 enhances glucose metabolism, leading to high activation of the sodium/hydrogen exchange for intracellular pH homeostasis.
Results highlight the regulatory role of BI-1 in idiopathic pulmonary fibrosis.
The effect of Bax Inhibitor-1(TMBIM6) as a regulatorof endoplasmic reticulum Ca2 (show CA2 ELISA Kits)+ homeostasis is regulated by intracellular pH by removing negative charges.
Constructed lentivirus expression vector for transfecting BI-1.
Data indicate that GAAP and BI-1 have a six membrane-spanning topology with cytosolic N and C termini and a C-terminal reentrant loop.
The results reveal BI-1 as a novel autophagy regulator that bridges Ca(2 (show CA2 ELISA Kits)) signaling between ER and mitochondria, reducing cellular oxygen consumption and contributing to cellular resilience in the face of metabolic stress.
The C terminus of Bax inhibitor-1 forms a Ca2 (show CA2 ELISA Kits)+-permeable channel pore.
BI-1 has a major role in the functioning of the adaptive immune system by regulating intracellular Ca(2 (show CA2 ELISA Kits)+) homeostasis in lymphocytes.
An endogenous protective role of BI-1 under conditions of chronic mild stress.
BI-1-induced ERK1/2 (show MAPK1/3 ELISA Kits) activation plays an important role in the modulation of intracellular reactive oxygen species generation and apoptotic cell death and may also affect autoimmune response.
BI-1-mediated enhancement of lysosomal activity regulates P450 (show POR ELISA Kits) 2E1 expression and resultant ROS (show ROS1 ELISA Kits) accumulation
highly maintained lysosomal activity may be one of the mechanisms by which BI-1 exerts its regulatory effects on the ER stress response and cell death.
A critical role of BI-1 as a stress integrator that modulates autophagy levels and other interconnected homeostatic processes.
BI-1 reduces endoplasmic reticulum (ER) stress and provides protection from acute brain injury via modulation of several ER-associated functions, including unfolded protein response signaling.
Suppressor of apoptosis
bax inhibitor 1
, testis enhanced gene transcript
, testis-enhanced gene transcript protein
, transmembrane BAX inhibitor motif-containing protein 6
, Bax inhibitor-1
, testis enhanced gene transcript (BAX inhibitor 1)