WB, IHC, IF/ICC, ELISA

Hm, Ms, Rt, Mk, Pg, Zf, Bv, Rb, Dg, Fs

货号	产品	规格	来源	应用	反应	文献引用
DF7742	PINK1 Ab	20ul	Rabbit	WB,IHC,IF/ICC	Hm,Ms,Rt	35
AF0235	Parkin Ab	20ul	Rabbit	WB,IHC	Hm,Ms,Rt	20
AF4650	LC3B Ab	20ul	Rabbit	WB,IHC,IF/ICC	Hm,Ms,Rt	33
AF5384	SQSTM1/p62 Ab	20ul	Rabbit	WB,IHC,IF/ICC	Hm,Ms,Rt,Mk	87
DF12360	CALCOCO2 Ab	20ul	Rabbit	WB,IHC,IF/ICC	Hm,Ms,Rt	2
DF8188	BNIP3 Ab	20ul	Rabbit	WB	Hm,Ms,Rt	7
AF0001	P-FUNDC1 (Ser17) Ab	20ul	Rabbit	WB	Hm	11
AF0002	FUNDC1 Ab	20ul	Rabbit	WB	Hm,Ms,Rt	1
AF7018	beta Actin Ab	20ul	Rabbit	WB,IHC,IF/ICC	Hm,Ms,Rt,Pg,Zf,Bv,Rb,Dg,Mk,Fs	747
S0001	Goat Anti-Rabbit IgG HRP	100ul	Goat	WB,IHC,ELISA	Rb	579

Mitophagy is a selective form of autophagy specifically targeting dysfunctional or damaged mitochondria for degradation. It plays a crucial role in maintaining mitochondrial quality control, cellular homeostasis, and preventing the accumulation of damaged mitochondria, which can lead to cellular dysfunction and contribute to the pathogenesis of various diseases.

Store at -20 °C. Stable for 12 months from date of receipt.

Mitophagy is a selective form of autophagy specifically targeting dysfunctional or damaged mitochondria for degradation. It plays a crucial role in maintaining mitochondrial quality control, cellular homeostasis, and preventing the accumulation of damaged mitochondria, which can lead to cellular dysfunction and contribute to the pathogenesis of various diseases.

The process of mitophagy involves several key steps:

1. **Recognition of damaged mitochondria:** Damaged mitochondria are recognized and tagged for degradation by specific molecular markers, such as phospho-ubiquitin and mitochondrial outer membrane proteins (e.g., PINK1 and Parkin).

2. **Recruitment of autophagy machinery:** Upon mitochondrial damage, the PTEN-induced kinase 1 (PINK1) accumulates on the outer mitochondrial membrane (OMM) and phosphorylates ubiquitin and Parkin, leading to the activation and recruitment of Parkin to damaged mitochondria. Parkin, an E3 ubiquitin ligase, ubiquitinates various OMM proteins, marking the damaged mitochondria for recognition by autophagic machinery.

3. **Engulfment by autophagosomes:** Ubiquitinated mitochondria are recognized by autophagy receptors, such as p62/SQSTM1 and Optineurin (OPTN), which bind both ubiquitin and LC3 on the forming autophagosome membrane. This facilitates the engulfment of damaged mitochondria by autophagosomes.

4. **Fusion with lysosomes and degradation:** The autophagosomes containing damaged mitochondria fuse with lysosomes, forming autolysosomes, where the engulfed mitochondria are degraded by lysosomal hydrolases, and the resulting breakdown products are recycled for cellular metabolism.

Key proteins involved in the mitophagy pathway include:

1. **PINK1 (PTEN-induced kinase 1):** PINK1 is a serine/threonine kinase that accumulates on the OMM of damaged mitochondria and phosphorylates ubiquitin and Parkin, initiating the recruitment of Parkin to damaged mitochondria.

2. **Parkin:** Parkin is an E3 ubiquitin ligase that is recruited to damaged mitochondria by PINK1 and catalyzes the ubiquitination of OMM proteins, leading to the recognition of damaged mitochondria by autophagic machinery.

3. **Autophagy receptors:** Autophagy receptors, such as p62/SQSTM1 and Optineurin (OPTN), bridge the interaction between ubiquitinated mitochondria and LC3 on the forming autophagosome membrane, facilitating the engulfment of damaged mitochondria by autophagosomes.

Mitophagy plays a critical role in maintaining mitochondrial homeostasis and cellular health by selectively removing dysfunctional or damaged mitochondria. Dysregulation of mitophagy has been implicated in various diseases, including neurodegenerative disorders, metabolic diseases, and cancer. Therefore, understanding the molecular mechanisms underlying mitophagy and the roles of key proteins involved in this process is essential for elucidating the pathogenesis of mitochondrial dysfunction-related diseases and for developing therapeutic strategies to target mitophagy for the treatment of these disorders.