acyl-CoA binding domain containing 5

acyl-CoA binding domain containing 7; Binds medium- and long-chain acyl-CoA esters

acyl-CoA binding domain containing 5

ubiquitin C

acyl-CoA binding domain containing 6; Binds long-chain acyl-coenzyme A molecules with a strong preference for unsaturated C18-1-CoA, lower affinity for unsaturated C20-4-CoA, and very weak affinity for saturated C16-0- CoA. Does not bind fatty acids

ubiquitin C

acyl-CoA binding domain containing 7; Binds medium- and long-chain acyl-CoA esters

acyl-CoA binding domain containing 5

acyl-CoA binding domain containing 7; Binds medium- and long-chain acyl-CoA esters

B-cell CLL/lymphoma 2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1)

acyl-CoA synthetase long-chain family member 3; Acyl-CoA synthetases (ACSL) activates long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. ACSL3 mediates hepatic lipogenesis (By similarity). Preferentially uses myristate, laurate, arachidonate and eicosapentaenoate as substrates (By similarity). Has mainly an anabolic role in energy metabolism. Required for the incorporation of fatty acids into phosphatidylcholine, the major phospholipid located on the surface of VLDL (very low density lipoproteins)

acyl-CoA synthetase long-chain family member 4; Activation of long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Preferentially uses arachidonate and eicosapentaenoate as substrates

acyl-CoA synthetase long-chain family member 3; Acyl-CoA synthetases (ACSL) activates long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. ACSL3 mediates hepatic lipogenesis (By similarity). Preferentially uses myristate, laurate, arachidonate and eicosapentaenoate as substrates (By similarity). Has mainly an anabolic role in energy metabolism. Required for the incorporation of fatty acids into phosphatidylcholine, the major phospholipid located on the surface of VLDL (very low density lipoproteins)

enoyl-CoA delta isomerase 2

acyl-CoA synthetase long-chain family member 3; Acyl-CoA synthetases (ACSL) activates long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. ACSL3 mediates hepatic lipogenesis (By similarity). Preferentially uses myristate, laurate, arachidonate and eicosapentaenoate as substrates (By similarity). Has mainly an anabolic role in energy metabolism. Required for the incorporation of fatty acids into phosphatidylcholine, the major phospholipid located on the surface of VLDL (very low density lipoproteins)

ubiquitin C

acyl-CoA synthetase long-chain family member 4; Activation of long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Preferentially uses arachidonate and eicosapentaenoate as substrates

acyl-CoA synthetase long-chain family member 3; Acyl-CoA synthetases (ACSL) activates long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. ACSL3 mediates hepatic lipogenesis (By similarity). Preferentially uses myristate, laurate, arachidonate and eicosapentaenoate as substrates (By similarity). Has mainly an anabolic role in energy metabolism. Required for the incorporation of fatty acids into phosphatidylcholine, the major phospholipid located on the surface of VLDL (very low density lipoproteins)

acyl-CoA synthetase long-chain family member 4; Activation of long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Preferentially uses arachidonate and eicosapentaenoate as substrates

enoyl-CoA delta isomerase 2

acyl-CoA synthetase long-chain family member 4; Activation of long-chain fatty acids for both synthesis of cellular lipids, and degradation via beta-oxidation. Preferentially uses arachidonate and eicosapentaenoate as substrates

ubiquitin C

annexin A4; Calcium/phospholipid-binding protein which promotes membrane fusion and is involved in exocytosis (By similarity)

caspase 3, apoptosis-related cysteine peptidase; Involved in the activation cascade of caspases responsible for apoptosis execution. At the onset of apoptosis it proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a ’216-Asp-|-Gly-217’ bond. Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop- helix leucine zipper domain and the membrane attachment domain. Cleaves and activates caspase-6, -7 and -9. Involved in the cleavage of huntingtin. Triggers cell adhesion in sympathetic neurons through RET cleavage

annexin A4; Calcium/phospholipid-binding protein which promotes membrane fusion and is involved in exocytosis (By similarity)

N-myristoyltransferase 2; Adds a myristoyl group to the N-terminal glycine residue of certain cellular proteins (By similarity)

annexin A4; Calcium/phospholipid-binding protein which promotes membrane fusion and is involved in exocytosis (By similarity)

tumor protein p53; Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression (By similarity)

annexin A4; Calcium/phospholipid-binding protein which promotes membrane fusion and is involved in exocytosis (By similarity)

ubiquitin C

B-cell CLL/lymphoma 2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1)

acyl-CoA binding domain containing 7; Binds medium- and long-chain acyl-CoA esters

B-cell CLL/lymphoma 2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1)

caspase 3, apoptosis-related cysteine peptidase; Involved in the activation cascade of caspases responsible for apoptosis execution. At the onset of apoptosis it proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a ’216-Asp-|-Gly-217’ bond. Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop- helix leucine zipper domain and the membrane attachment domain. Cleaves and activates caspase-6, -7 and -9. Involved in the cleavage of huntingtin. Triggers cell adhesion in sympathetic neurons through RET cleavage

B-cell CLL/lymphoma 2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1)

diazepam binding inhibitor (GABA receptor modulator, acyl-CoA binding protein)

B-cell CLL/lymphoma 2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1)

N-myristoyltransferase 2; Adds a myristoyl group to the N-terminal glycine residue of certain cellular proteins (By similarity)

B-cell CLL/lymphoma 2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1)

tumor protein p53; Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression (By similarity)