FZR1 Antibody [E11J24] | Primary Antibodies

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:100-1:1000 IP1:100-1:200 IHC1:50-1:500 IF1:50-1:500

Application
WB, IP, IHC, IF, ELISA

Reactivity
Human, Mouse, Rat

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
55 kDa

Datasheet & SDS

Biological Description

Specificity
FZR1 Antibody [E11J24] detects endogenous levels of total FZR1 protein.

Clone
E11J24

Synonym(s)
Fizzy-related protein homolog, Fzr, CDC20-like protein 1, Cdh1/Hct1 homolog (Hcdh1), FZR1, CDH1, FYR, FZR, KIAA1242

Background
FZR1, also known as CDH1, is a WD-repeat–containing coactivator of the anaphase-promoting complex/cyclosome (APC/C) E3 ubiquitin ligase. It acts as a substrate-selective adapter, linking APC/C activity to the temporal regulation of cyclins, mitotic regulators, and DNA damage–response factors during mitosis, G1, and the G2 checkpoint. FZR1 contains multiple WD40 repeats forming a β-propeller domain that recognizes degron motifs in substrates, and its N-terminal regulatory sites are phosphorylated by various kinases to modulate its interaction and activity with APC/C throughout the cell cycle. FZR1 binds the APC/C core in late mitosis and G1, directing ubiquitination of substrates such as mitotic cyclins, Aurora kinase A, PLK1, Skp2, and CtIP/RBBP8. This prevents premature accumulation of positive cell-cycle regulators, maintains low CDK activity in G1, and influences the choice between non-homologous end joining and homologous recombination during DNA double-strand break repair. Loss of FZR1 function in human and mouse somatic cells shortens G1, prolongs S phase, and leads to DNA damage accumulation and impaired proliferation without blocking mitotic exit, indicating that APC/C^FZR1 activity is dispensable for completion of mitosis but required for proper G1 control and efficient DNA replication. FZR1 also regulates the timing of meiosis I spindle assembly, supports maintenance of prophase I arrest, and prevents chromosome nondisjunction by targeting specific meiotic regulators for degradation; FZR1 insufficiency accelerates meiosis I and increases segregation errors. At the G2 DNA-damage checkpoint, FZR1 is dephosphorylated and reassociates with APC/C, promoting PLK1 ubiquitination and restraining mitotic entry, and, through CtIP turnover, participates in pathway choice for double-strand break repair and checkpoint enforcement. FZR1 regulates quiescence and self-renewal in hematopoietic stem cells by promoting ubiquitination of RUNX1 at defined lysines; FZR1 insufficiency leads to RUNX1 accumulation, disturbed quiescence, and altered stem-cell homeostasis. In cancer signaling, APC/C^FZR1 targets BRAF for degradation and restricts MAPK pathway output, with reduced FZR1 activity being associated with enhanced BRAF signaling and increased tumorigenic potential in melanoma models.

Background

FZR1, also known as CDH1, is a WD-repeat–containing coactivator of the anaphase-promoting complex/cyclosome (APC/C) E3 ubiquitin ligase. It acts as a substrate-selective adapter, linking APC/C activity to the temporal regulation of cyclins, mitotic regulators, and DNA damage–response factors during mitosis, G1, and the G2 checkpoint. FZR1 contains multiple WD40 repeats forming a β-propeller domain that recognizes degron motifs in substrates, and its N-terminal regulatory sites are phosphorylated by various kinases to modulate its interaction and activity with APC/C throughout the cell cycle. FZR1 binds the APC/C core in late mitosis and G1, directing ubiquitination of substrates such as mitotic cyclins, Aurora kinase A, PLK1, Skp2, and CtIP/RBBP8. This prevents premature accumulation of positive cell-cycle regulators, maintains low CDK activity in G1, and influences the choice between non-homologous end joining and homologous recombination during DNA double-strand break repair. Loss of FZR1 function in human and mouse somatic cells shortens G1, prolongs S phase, and leads to DNA damage accumulation and impaired proliferation without blocking mitotic exit, indicating that APC/C^FZR1 activity is dispensable for completion of mitosis but required for proper G1 control and efficient DNA replication. FZR1 also regulates the timing of meiosis I spindle assembly, supports maintenance of prophase I arrest, and prevents chromosome nondisjunction by targeting specific meiotic regulators for degradation; FZR1 insufficiency accelerates meiosis I and increases segregation errors. At the G2 DNA-damage checkpoint, FZR1 is dephosphorylated and reassociates with APC/C, promoting PLK1 ubiquitination and restraining mitotic entry, and, through CtIP turnover, participates in pathway choice for double-strand break repair and checkpoint enforcement. FZR1 regulates quiescence and self-renewal in hematopoietic stem cells by promoting ubiquitination of RUNX1 at defined lysines; FZR1 insufficiency leads to RUNX1 accumulation, disturbed quiescence, and altered stem-cell homeostasis. In cancer signaling, APC/C^FZR1 targets BRAF for degradation and restricts MAPK pathway output, with reduced FZR1 activity being associated with enhanced BRAF signaling and increased tumorigenic potential in melanoma models.

References
https://pubmed.ncbi.nlm.nih.gov/19861496/ https://pubmed.ncbi.nlm.nih.gov/28174173/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%