- published: 25 Feb 2019
- views: 58048
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Bcl-2-associated X protein
Apoptosis regulator BAX, also known as bcl-2-like protein 4, is a protein that in humans is encoded by the BAX gene. BAX is a member of the Bcl-2 gene family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to the loss in membrane potential and the release of cytochrome c. The expression of this gene is regulated by the tumor suppressor P53 and has been shown to be involved in P53-mediated apoptosis.
Structure
The BAX gene was the first identified pro-apoptotic member of the Bcl-2 protein family. Bcl-2 family members share one or more of the four characteristic domains of homology entitled the Bcl-2 homology (BH) domains (named BH1, BH2, BH3 and BH4), and can form hetero- or homodimers. These domains are composed of nine α-helices, with a hydrophobic α-helix core surrounded by amphipathic helices and a transmembrane C-terminal α-helix anchored to the mitochondrial outer membrane (MOM). A hydrophobic groove formed along the C-terminal of α2 to the N-terminal of α5, and some residues from α8, binds the BH3 domain of other BAX or BCL-2 proteins in its active form. In the protein’s inactive form, the groove binds its transmembrane domain, transitioning it from a membrane-bound to a cytosolic protein. A smaller hydrophobic groove formed by the α1 and α6 helices is located on the opposite side of the protein from the major groove, and may serve as a BAX activation site.
This page contains text from Wikipedia, the Free Encyclopedia - https://wn.com/Bcl-2-associated_X_protein
Podcasts:
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Apoptosis Regulation by Genes | Bcl-2 Family
In this video we have discussed the regulation of Apoptosis by genes. The Apoptosis is regulated by various genes but Bcl family of genes are the primary regulators of the apoptosis. Apoptosis (from Ancient Greek ἀπόπτωσις "falling off") is a form of programmed cell death that occurs in multicellular organisms.[2] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and global[vague] mRNA decay. The initiation of apoptosis is tightly regulated by activation mechanisms, because once apoptosis has begun, it inevitably leads to the death of the cell. The two best-understood activation mechanisms are the intrinsic pathway (also called the mi...
published: 25 Feb 2019 -
Medical vocabulary: What does bcl-2-Associated X Protein mean
What does bcl-2-Associated X Protein mean in English?
published: 20 Jan 2016 -
1 7 Lecture 6 The Bcl 2 superfamily 12 06
Coursera Programmed Cell Death (PCD) course by Barbara Conradt, Module 1 The course will cover the following topics: 1. Introduction to programmed cell death and apoptosis 2. The BCL-2 family of proteins 3. Apaf proteins 4. Caspases 5. Mechanisms that regulate apoptosis 6. Non-apoptotic functions of components of the central apoptosis machinery 7. Diseases caused by deregulated apoptosis
published: 27 May 2016 -
Mechanism of Cytochrome C Release from Mitochondria
In this video we have discussed the release of Cytochrome C from Mitochondria. You know upon the Apoptotic signals the cell prepares itself to self destruct . The intrinsic way of Apoptosis is the pathway which mediates the release of Cytochrome C release from Mitochondria. The Cytochrome C is found to be trapped in the internal membrane of Mitochondria where it is bound to the lipids (cardiolipin ) of the membrane. So in order to release the Cytochrome c we need lipid peroxidation so that it is released and then we need to transport it to the outside of mitochondria and to do this the external membrane is to be permeable for this cytochrome c . The pore is formed on the membrane with the help form BAX and BAK proteins. During the early phase of apoptosis, mitochondrial ROS production is s...
published: 04 Mar 2019 -
The BCL2 protein family; structure and mechanism of apoptotic cell death
published: 17 Mar 2021 -
Bcl-xL
Bcl-xL, by Wikipedia https://en.wikipedia.org/wiki?curid=10029222 / CC BY SA 3.0 #Mitochondria #Cancer_research #Apoptosis X-ray crystal structure of Bcl-xL with 1. 76 Å resolution B-cell lymphoma-extra large （Bcl-xL）, encoded by the BCL2-like 1 gene, is a transmembrane molecule in the mitochondria. It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of mitochondrial contents such as cytochrome c, which leads to caspase activation and ultimately, programmed cell death. It is a well-established concept in the field of apoptosis that relative amounts of pro- and anti-survival Bcl-2 family of proteins determine whether the cell will undergo cell death; if more Bcl-xL is present, then pores are non-permeable to pro-apoptotic molecule...
published: 08 Jan 2022
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5:23
Apoptosis Regulation by Genes | Bcl-2 Family
- Order: Reorder
- Duration: 5:23
- Uploaded Date: 25 Feb 2019
- views: 58048
In this video we have discussed the regulation of Apoptosis by genes.
The Apoptosis is regulated by various genes but Bcl family of genes are the primary regul...
In this video we have discussed the regulation of Apoptosis by genes.
The Apoptosis is regulated by various genes but Bcl family of genes are the primary regulators of the apoptosis.
Apoptosis (from Ancient Greek ἀπόπτωσις "falling off") is a form of programmed cell death that occurs in multicellular organisms.[2] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and global[vague] mRNA decay.
The initiation of apoptosis is tightly regulated by activation mechanisms, because once apoptosis has begun, it inevitably leads to the death of the cell. The two best-understood activation mechanisms are the intrinsic pathway (also called the mitochondrial pathway) and the extrinsic pathway.
https://wn.com/Apoptosis_Regulation_By_Genes_|_Bcl_2_Family
In this video we have discussed the regulation of Apoptosis by genes.
The Apoptosis is regulated by various genes but Bcl family of genes are the primary regulators of the apoptosis.
Apoptosis (from Ancient Greek ἀπόπτωσις "falling off") is a form of programmed cell death that occurs in multicellular organisms.[2] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and global[vague] mRNA decay.
The initiation of apoptosis is tightly regulated by activation mechanisms, because once apoptosis has begun, it inevitably leads to the death of the cell. The two best-understood activation mechanisms are the intrinsic pathway (also called the mitochondrial pathway) and the extrinsic pathway.
0:28
Medical vocabulary: What does bcl-2-Associated X Protein mean
- Order: Reorder
- Duration: 0:28
- Uploaded Date: 20 Jan 2016
- views: 12
What does bcl-2-Associated X Protein mean in English?
What does bcl-2-Associated X Protein mean in English?
https://wn.com/Medical_Vocabulary_What_Does_Bcl_2_Associated_X_Protein_Mean
What does bcl-2-Associated X Protein mean in English?
- published: 20 Jan 2016
- views: 12
12:07
1 7 Lecture 6 The Bcl 2 superfamily 12 06
- Order: Reorder
- Duration: 12:07
- Uploaded Date: 27 May 2016
- views: 2603
Coursera Programmed Cell Death (PCD) course by Barbara Conradt, Module 1
The course will cover the following topics:
1. Introduction to programmed cell dea...
Coursera Programmed Cell Death (PCD) course by Barbara Conradt, Module 1
The course will cover the following topics:
1. Introduction to programmed cell death and apoptosis
2. The BCL-2 family of proteins
3. Apaf proteins
4. Caspases
5. Mechanisms that regulate apoptosis
6. Non-apoptotic functions of components of the central apoptosis machinery
7. Diseases caused by deregulated apoptosis
https://wn.com/1_7_Lecture_6_The_Bcl_2_Superfamily_12_06
Coursera Programmed Cell Death (PCD) course by Barbara Conradt, Module 1
The course will cover the following topics:
1. Introduction to programmed cell death and apoptosis
2. The BCL-2 family of proteins
3. Apaf proteins
4. Caspases
5. Mechanisms that regulate apoptosis
6. Non-apoptotic functions of components of the central apoptosis machinery
7. Diseases caused by deregulated apoptosis
- published: 27 May 2016
- views: 2603
3:20
Mechanism of Cytochrome C Release from Mitochondria
- Order: Reorder
- Duration: 3:20
- Uploaded Date: 04 Mar 2019
- views: 22966
In this video we have discussed the release of Cytochrome C from Mitochondria. You know upon the Apoptotic signals the cell prepares itself to self destruct . T...
In this video we have discussed the release of Cytochrome C from Mitochondria. You know upon the Apoptotic signals the cell prepares itself to self destruct . The intrinsic way of Apoptosis is the pathway which mediates the release of Cytochrome C release from Mitochondria.
The Cytochrome C is found to be trapped in the internal membrane of Mitochondria where it is bound to the lipids (cardiolipin ) of the membrane.
So in order to release the Cytochrome c we need lipid peroxidation so that it is released and then we need to transport it to the outside of mitochondria and to do this the external membrane is to be permeable for this cytochrome c . The pore is formed on the membrane with the help form BAX and BAK proteins.
During the early phase of apoptosis, mitochondrial ROS production is stimulated, and cardiolipin is oxidized by a peroxidase function of the cardiolipin–cytochrome c complex. The hemoprotein is then detached from the mitochondrial inner membrane and can be extruded into the soluble cytoplasm through pores in the outer membrane.
https://wn.com/Mechanism_Of_Cytochrome_C_Release_From_Mitochondria
In this video we have discussed the release of Cytochrome C from Mitochondria. You know upon the Apoptotic signals the cell prepares itself to self destruct . The intrinsic way of Apoptosis is the pathway which mediates the release of Cytochrome C release from Mitochondria.
The Cytochrome C is found to be trapped in the internal membrane of Mitochondria where it is bound to the lipids (cardiolipin ) of the membrane.
So in order to release the Cytochrome c we need lipid peroxidation so that it is released and then we need to transport it to the outside of mitochondria and to do this the external membrane is to be permeable for this cytochrome c . The pore is formed on the membrane with the help form BAX and BAK proteins.
During the early phase of apoptosis, mitochondrial ROS production is stimulated, and cardiolipin is oxidized by a peroxidase function of the cardiolipin–cytochrome c complex. The hemoprotein is then detached from the mitochondrial inner membrane and can be extruded into the soluble cytoplasm through pores in the outer membrane.
- published: 04 Mar 2019
- views: 22966
1:20:43
The BCL2 protein family; structure and mechanism of apoptotic cell death
- Order: Reorder
- Duration: 1:20:43
- Uploaded Date: 17 Mar 2021
- views: 1501
- published: 17 Mar 2021
- views: 1501
3:31
Bcl-xL
- Order: Reorder
- Duration: 3:31
- Uploaded Date: 08 Jan 2022
- views: 66
Bcl-xL, by Wikipedia https://en.wikipedia.org/wiki?curid=10029222 / CC BY SA 3.0
#Mitochondria
#Cancer_research
#Apoptosis
X-ray crystal structure of Bcl-xL wi...
Bcl-xL, by Wikipedia https://en.wikipedia.org/wiki?curid=10029222 / CC BY SA 3.0
#Mitochondria
#Cancer_research
#Apoptosis
X-ray crystal structure of Bcl-xL with 1.
76 Å resolution B-cell lymphoma-extra large （Bcl-xL）, encoded by the BCL2-like 1 gene, is a transmembrane molecule in the mitochondria.
It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of mitochondrial contents such as cytochrome c, which leads to caspase activation and ultimately, programmed cell death.
It is a well-established concept in the field of apoptosis that relative amounts of pro- and anti-survival Bcl-2 family of proteins determine whether the cell will undergo cell death; if more Bcl-xL is present,
then pores are non-permeable to pro-apoptotic molecules and the cell survives.
However, if Bax and Bak become activated, and Bcl-xL is sequestered away by gatekeeper BH3-only factors （e.g. Bim） causing a pore to form, cytochrome c is released leading to initiation of caspase cascade and apoptotic events.
While the exact signaling pathway of Bcl-xL is still not known, it is believed that Bcl-xL differs highly from Bcl-2 in their mechanism of inducing apoptosis.
Bcl-xL is about ten times more functional than Bcl-2 when induced by the chemotherapy drug, Doxorubicin and can specifically bind to cytochrome C residues, preventing apoptosis.
It can also prevent the formation of Apaf-1 and Caspase 9 complex by acting directly upon Apaf-1 rather than Caspase 9, as shown in nematode homologs.
Overview of signal transduction pathways Bcl-xL dysfunction in mice can cause ineffective production of red blood cells, severe anemia, hemolysis, and death.
This protein has also been shown as a requirement for heme production and in erythroid lineage, Bcl-xL is a major survival factor responsible
for an estimated half of the total survival "signal" proerythroblasts must receive in order to survive and become red cells.
Bcl-xL promoter contains GATA-1 and...
https://wn.com/Bcl_Xl
Bcl-xL, by Wikipedia https://en.wikipedia.org/wiki?curid=10029222 / CC BY SA 3.0
#Mitochondria
#Cancer_research
#Apoptosis
X-ray crystal structure of Bcl-xL with 1.
76 Å resolution B-cell lymphoma-extra large （Bcl-xL）, encoded by the BCL2-like 1 gene, is a transmembrane molecule in the mitochondria.
It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of mitochondrial contents such as cytochrome c, which leads to caspase activation and ultimately, programmed cell death.
It is a well-established concept in the field of apoptosis that relative amounts of pro- and anti-survival Bcl-2 family of proteins determine whether the cell will undergo cell death; if more Bcl-xL is present,
then pores are non-permeable to pro-apoptotic molecules and the cell survives.
However, if Bax and Bak become activated, and Bcl-xL is sequestered away by gatekeeper BH3-only factors （e.g. Bim） causing a pore to form, cytochrome c is released leading to initiation of caspase cascade and apoptotic events.
While the exact signaling pathway of Bcl-xL is still not known, it is believed that Bcl-xL differs highly from Bcl-2 in their mechanism of inducing apoptosis.
Bcl-xL is about ten times more functional than Bcl-2 when induced by the chemotherapy drug, Doxorubicin and can specifically bind to cytochrome C residues, preventing apoptosis.
It can also prevent the formation of Apaf-1 and Caspase 9 complex by acting directly upon Apaf-1 rather than Caspase 9, as shown in nematode homologs.
Overview of signal transduction pathways Bcl-xL dysfunction in mice can cause ineffective production of red blood cells, severe anemia, hemolysis, and death.
This protein has also been shown as a requirement for heme production and in erythroid lineage, Bcl-xL is a major survival factor responsible
for an estimated half of the total survival "signal" proerythroblasts must receive in order to survive and become red cells.
Bcl-xL promoter contains GATA-1 and...
- published: 08 Jan 2022
- views: 66
5:23
Apoptosis Regulation by Genes | Bcl-2 Family
In this video we have discussed the regulation of Apoptosis by genes.
The Apoptosis is re...
published: 25 Feb 2019
Apoptosis Regulation by Genes | Bcl-2 Family
Apoptosis Regulation by Genes | Bcl-2 Family
- Report rights infringement
- published: 25 Feb 2019
- views: 58048
In this video we have discussed the regulation of Apoptosis by genes.
The Apoptosis is regulated by various genes but Bcl family of genes are the primary regulators of the apoptosis.
Apoptosis (from Ancient Greek ἀπόπτωσις "falling off") is a form of programmed cell death that occurs in multicellular organisms.[2] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and global[vague] mRNA decay.
The initiation of apoptosis is tightly regulated by activation mechanisms, because once apoptosis has begun, it inevitably leads to the death of the cell. The two best-understood activation mechanisms are the intrinsic pathway (also called the mitochondrial pathway) and the extrinsic pathway.
0:28
Medical vocabulary: What does bcl-2-Associated X Protein mean
What does bcl-2-Associated X Protein mean in English?
published: 20 Jan 2016
Medical vocabulary: What does bcl-2-Associated X Protein mean
Medical vocabulary: What does bcl-2-Associated X Protein mean
- Report rights infringement
- published: 20 Jan 2016
- views: 12
What does bcl-2-Associated X Protein mean in English?
12:07
1 7 Lecture 6 The Bcl 2 superfamily 12 06
Coursera Programmed Cell Death (PCD) course by Barbara Conradt, Module 1
The course will c...
published: 27 May 2016
1 7 Lecture 6 The Bcl 2 superfamily 12 06
1 7 Lecture 6 The Bcl 2 superfamily 12 06
- Report rights infringement
- published: 27 May 2016
- views: 2603
Coursera Programmed Cell Death (PCD) course by Barbara Conradt, Module 1
The course will cover the following topics:
1. Introduction to programmed cell death and apoptosis
2. The BCL-2 family of proteins
3. Apaf proteins
4. Caspases
5. Mechanisms that regulate apoptosis
6. Non-apoptotic functions of components of the central apoptosis machinery
7. Diseases caused by deregulated apoptosis
3:20
Mechanism of Cytochrome C Release from Mitochondria
In this video we have discussed the release of Cytochrome C from Mitochondria. You know up...
published: 04 Mar 2019
Mechanism of Cytochrome C Release from Mitochondria
Mechanism of Cytochrome C Release from Mitochondria
- Report rights infringement
- published: 04 Mar 2019
- views: 22966
In this video we have discussed the release of Cytochrome C from Mitochondria. You know upon the Apoptotic signals the cell prepares itself to self destruct . The intrinsic way of Apoptosis is the pathway which mediates the release of Cytochrome C release from Mitochondria.
The Cytochrome C is found to be trapped in the internal membrane of Mitochondria where it is bound to the lipids (cardiolipin ) of the membrane.
So in order to release the Cytochrome c we need lipid peroxidation so that it is released and then we need to transport it to the outside of mitochondria and to do this the external membrane is to be permeable for this cytochrome c . The pore is formed on the membrane with the help form BAX and BAK proteins.
During the early phase of apoptosis, mitochondrial ROS production is stimulated, and cardiolipin is oxidized by a peroxidase function of the cardiolipin–cytochrome c complex. The hemoprotein is then detached from the mitochondrial inner membrane and can be extruded into the soluble cytoplasm through pores in the outer membrane.
1:20:43
The BCL2 protein family; structure and mechanism of apoptotic cell death
published: 17 Mar 2021
The BCL2 protein family; structure and mechanism of apoptotic cell death
The BCL2 protein family; structure and mechanism of apoptotic cell death
- Report rights infringement
- published: 17 Mar 2021
- views: 1501
3:31
Bcl-xL
Bcl-xL, by Wikipedia https://en.wikipedia.org/wiki?curid=10029222 / CC BY SA 3.0
#Mitocho...
published: 08 Jan 2022
Bcl-xL
Bcl-xL
- Report rights infringement
- published: 08 Jan 2022
- views: 66
Bcl-xL, by Wikipedia https://en.wikipedia.org/wiki?curid=10029222 / CC BY SA 3.0
#Mitochondria
#Cancer_research
#Apoptosis
X-ray crystal structure of Bcl-xL with 1.
76 Å resolution B-cell lymphoma-extra large （Bcl-xL）, encoded by the BCL2-like 1 gene, is a transmembrane molecule in the mitochondria.
It is a member of the Bcl-2 family of proteins, and acts as an anti-apoptotic protein by preventing the release of mitochondrial contents such as cytochrome c, which leads to caspase activation and ultimately, programmed cell death.
It is a well-established concept in the field of apoptosis that relative amounts of pro- and anti-survival Bcl-2 family of proteins determine whether the cell will undergo cell death; if more Bcl-xL is present,
then pores are non-permeable to pro-apoptotic molecules and the cell survives.
However, if Bax and Bak become activated, and Bcl-xL is sequestered away by gatekeeper BH3-only factors （e.g. Bim） causing a pore to form, cytochrome c is released leading to initiation of caspase cascade and apoptotic events.
While the exact signaling pathway of Bcl-xL is still not known, it is believed that Bcl-xL differs highly from Bcl-2 in their mechanism of inducing apoptosis.
Bcl-xL is about ten times more functional than Bcl-2 when induced by the chemotherapy drug, Doxorubicin and can specifically bind to cytochrome C residues, preventing apoptosis.
It can also prevent the formation of Apaf-1 and Caspase 9 complex by acting directly upon Apaf-1 rather than Caspase 9, as shown in nematode homologs.
Overview of signal transduction pathways Bcl-xL dysfunction in mice can cause ineffective production of red blood cells, severe anemia, hemolysis, and death.
This protein has also been shown as a requirement for heme production and in erythroid lineage, Bcl-xL is a major survival factor responsible
for an estimated half of the total survival "signal" proerythroblasts must receive in order to survive and become red cells.
Bcl-xL promoter contains GATA-1 and...
Bcl-2-associated X protein
Apoptosis regulator BAX, also known as bcl-2-like protein 4, is a protein that in humans is encoded by the BAX gene. BAX is a member of the Bcl-2 gene family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to the loss in membrane potential and the release of cytochrome c. The expression of this gene is regulated by the tumor suppressor P53 and has been shown to be involved in P53-mediated apoptosis.
Structure
The BAX gene was the first identified pro-apoptotic member of the Bcl-2 protein family. Bcl-2 family members share one or more of the four characteristic domains of homology entitled the Bcl-2 homology (BH) domains (named BH1, BH2, BH3 and BH4), and can form hetero- or homodimers. These domains are composed of nine α-helices, with a hydrophobic α-helix core surrounded by amphipathic helices and a transmembrane C-terminal α-helix anchored to the mitochondrial outer membrane (MOM). A hydrophobic groove formed along the C-terminal of α2 to the N-terminal of α5, and some residues from α8, binds the BH3 domain of other BAX or BCL-2 proteins in its active form. In the protein’s inactive form, the groove binds its transmembrane domain, transitioning it from a membrane-bound to a cytosolic protein. A smaller hydrophobic groove formed by the α1 and α6 helices is located on the opposite side of the protein from the major groove, and may serve as a BAX activation site.
This page contains text from Wikipedia, the Free Encyclopedia - https://wn.com/Bcl-2-associated_X_protein
Apoptosis Regulation by Genes | Bcl-2 Family...
Medical vocabulary: What does bcl-2-Associated X P...
1 7 Lecture 6 The Bcl 2 superfamily 12 06...
Mechanism of Cytochrome C Release from Mitochondri...
The BCL2 protein family; structure and mechanism o...
Bcl-xL...
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