Necroptosis Antibody Sampler Kit - #KF2032
产品描述
货号:
KF2032
产品:
Necroptosis Antibody Sampler Kit
应用:
WB, IHC, IF/ICC, ELISA
反应:
Hm, Ms, Rt, Pg, Bv, Gt, Mk, Ck, Rb
产品包含:
货号 | 产品 | 规格 | 来源 | 应用 | 反应 | 文献引用 |
---|---|---|---|---|---|---|
AF7877 | RIPK1 Ab | 20ul | Rabbit | WB | Hm,Ms,Rt | 8 |
AF2398 | P-RIPK1 (Ser166) Ab | 20ul | Rabbit | WB,IHC,IF/ICC | Hm,Ms | 4 |
DF7412 | MLKL Ab | 20ul | Rabbit | WB,IHC,IF/ICC | Hm,Ms,Rt | 22 |
AF7420 | P-MLKL (Ser358) Ab | 20ul | Rabbit | WB,IHC | Hm,Ms,Rt | 34 |
AF7942 | RIP3 Ab | 20ul | Rabbit | WB,IHC | Hm,Ms,Rt | 11 |
AF3893 | P-RIPK3 (Ser227) Ab | 20ul | Rabbit | IHC | Hm,Rt | 0 |
AF7021 | GAPDH Ab | 20ul | Rabbit | WB,IHC,IF/ICC | Hm,Ms,Rt,Pg,Bv,Gt,Mk,Ck | 757 |
S0001 | Goat Anti-Rabbit IgG HRP | 100ul | Goat | WB,IHC,ELISA | Rb | 506 |
简介:
Necroptosis is a form of programmed cell death that shares features with both apoptosis and necrosis. It is initiated by a specific signaling cascade and is characterized by cellular swelling, plasma membrane rupture, and the release of intracellular contents, leading to inflammation and immune responses.
储存条件:
Store at -20 °C. Stable for 12 months from date of receipt.
Necroptosis is a form of programmed cell death that shares features with both apoptosis and necrosis. It is initiated by a specific signaling cascade and is characterized by cellular swelling, plasma membrane rupture, and the release of intracellular contents, leading to inflammation and immune responses.
The necroptosis pathway is primarily mediated by the receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3), as well as by mixed lineage kinase domain-like protein (MLKL).
1. **Initiation:** Necroptosis can be triggered by various extracellular signals, including activation of death receptors (e.g., TNF receptor 1), Toll-like receptors, or pattern recognition receptors. Under certain conditions, when caspase-8 activity is inhibited or deficient, RIPK1 forms a complex with RIPK3 via their RIP homotypic interaction motif (RHIM) domains, leading to the activation of RIPK3.
2. **Activation of RIPK3:** Activated RIPK3 phosphorylates MLKL, leading to its oligomerization and translocation to the plasma membrane.
3. **Plasma membrane disruption:** Oligomerized and phosphorylated MLKL disrupts the integrity of the plasma membrane, leading to cellular swelling and plasma membrane rupture, ultimately resulting in necroptotic cell death.
Key proteins involved in the necroptosis pathway include:
1. **Receptor-interacting protein kinase 1 (RIPK1):** RIPK1 is a serine/threonine kinase that plays a central role in regulating cell death and inflammation. It is recruited to death receptors and mediates signaling pathways that lead to apoptosis, necroptosis, or survival, depending on the cellular context.
2. **Receptor-interacting protein kinase 3 (RIPK3):** RIPK3 is a closely related kinase to RIPK1 and forms a complex with RIPK1 under conditions of caspase-8 inhibition or deficiency. Activated RIPK3 phosphorylates MLKL, leading to necroptotic cell death.
3. **Mixed lineage kinase domain-like protein (MLKL):** MLKL is the effector protein of necroptosis. Phosphorylated MLKL undergoes conformational changes and translocates to the plasma membrane, where it disrupts membrane integrity and induces necroptotic cell death.
Necroptosis plays a critical role in various physiological and pathological processes, including development, immune responses, and tissue injury. Dysregulation of necroptosis has been implicated in various diseases, including inflammatory disorders, neurodegenerative diseases, ischemia-reperfusion injury, and infectious diseases. Therefore, understanding the molecular mechanisms underlying necroptosis and the roles of key proteins involved in this process is essential for elucidating the pathogenesis of these diseases and for developing therapeutic strategies to target necroptosis for the treatment of these disorders.
The necroptosis pathway is primarily mediated by the receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3), as well as by mixed lineage kinase domain-like protein (MLKL).
1. **Initiation:** Necroptosis can be triggered by various extracellular signals, including activation of death receptors (e.g., TNF receptor 1), Toll-like receptors, or pattern recognition receptors. Under certain conditions, when caspase-8 activity is inhibited or deficient, RIPK1 forms a complex with RIPK3 via their RIP homotypic interaction motif (RHIM) domains, leading to the activation of RIPK3.
2. **Activation of RIPK3:** Activated RIPK3 phosphorylates MLKL, leading to its oligomerization and translocation to the plasma membrane.
3. **Plasma membrane disruption:** Oligomerized and phosphorylated MLKL disrupts the integrity of the plasma membrane, leading to cellular swelling and plasma membrane rupture, ultimately resulting in necroptotic cell death.
Key proteins involved in the necroptosis pathway include:
1. **Receptor-interacting protein kinase 1 (RIPK1):** RIPK1 is a serine/threonine kinase that plays a central role in regulating cell death and inflammation. It is recruited to death receptors and mediates signaling pathways that lead to apoptosis, necroptosis, or survival, depending on the cellular context.
2. **Receptor-interacting protein kinase 3 (RIPK3):** RIPK3 is a closely related kinase to RIPK1 and forms a complex with RIPK1 under conditions of caspase-8 inhibition or deficiency. Activated RIPK3 phosphorylates MLKL, leading to necroptotic cell death.
3. **Mixed lineage kinase domain-like protein (MLKL):** MLKL is the effector protein of necroptosis. Phosphorylated MLKL undergoes conformational changes and translocates to the plasma membrane, where it disrupts membrane integrity and induces necroptotic cell death.
Necroptosis plays a critical role in various physiological and pathological processes, including development, immune responses, and tissue injury. Dysregulation of necroptosis has been implicated in various diseases, including inflammatory disorders, neurodegenerative diseases, ischemia-reperfusion injury, and infectious diseases. Therefore, understanding the molecular mechanisms underlying necroptosis and the roles of key proteins involved in this process is essential for elucidating the pathogenesis of these diseases and for developing therapeutic strategies to target necroptosis for the treatment of these disorders.
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