Cdc6 Antibody [L3E6] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 - 1:10000 IF1:100

Application
WB, IF

Reactivity
Human

Source
Rabbit 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
63 kDa

Positive Control	Human breast carcinoma tissue; Human thyroid cancer tissue; Human gastric adenocarcinoma tissue; 293T cells (Hydroxyurea, 20mM, 24 h); HeLa cells; HCT116 cells (Hydtoxyurea, 1mM, 16 h)
Negative Control

Datasheet & SDS

Biological Description

Specificity
Cdc6 Antibody [L3E6] detects endogenous levels of total Cdc6 protein.

Clone
L3E6

Synonym(s)
CDC18L; CDC6; Cell division control protein 6 homolog; CDC6-related protein; Cdc18-related protein; p62(cdc6); HsCdc18; HsCDC6

Background
Cdc6, or Cell Division Cycle 6, is an AAA+ ATPase that plays a critical role in initiating eukaryotic DNA replication. It is primarily expressed in the nucleus of proliferating cells and is tightly regulated during the G1 phase of the cell cycle. Cdc6 contains an N-terminal winged-helix domain that facilitates binding to the origin recognition complex, a central AAA+ ATPase domain with Walker A and B motifs necessary for ATP-dependent loading of the MCM helicase, and a C-terminal zinc-finger domain. Key residues within the ATP-binding pocket and the surfaces that interact with ORC coordinate the hexamerization of the MCM2-7 helicase complex around DNA. After mitosis, Cdc6 binds to ORC at replication origins, recruits Cdt1, and assists in loading two MCM2-7 hexamers to form the pre-replicative complex. ATP hydrolysis by Cdc6 is required to remodel the MCM complex for bidirectional helicase activation at the G1/S transition, thereby ensuring that replication origins are licensed only once per cell cycle. As an E2F transcriptional target, Cdc6 serves as a link between mitogenic signaling and replication licensing, coordinates with cyclin-dependent kinases and Cdc7 for origin firing, and upholds checkpoints that prevent DNA re-replication. Following the S phase, Cdc6 is degraded through the ubiquitin-proteasome pathway to reset replication licensing. Dysregulation of Cdc6 drives oncogenesis, as its overexpression in cancers such as colorectal, lung, and cervical tumors enhances proliferation through interactions with cyclins and induces replication stress, while mutations can lead to genomic instability. Cdc6 is also involved in suppressing mitosis and activating cell cycle checkpoints.

Background

Cdc6, or Cell Division Cycle 6, is an AAA+ ATPase that plays a critical role in initiating eukaryotic DNA replication. It is primarily expressed in the nucleus of proliferating cells and is tightly regulated during the G1 phase of the cell cycle. Cdc6 contains an N-terminal winged-helix domain that facilitates binding to the origin recognition complex, a central AAA+ ATPase domain with Walker A and B motifs necessary for ATP-dependent loading of the MCM helicase, and a C-terminal zinc-finger domain. Key residues within the ATP-binding pocket and the surfaces that interact with ORC coordinate the hexamerization of the MCM2-7 helicase complex around DNA. After mitosis, Cdc6 binds to ORC at replication origins, recruits Cdt1, and assists in loading two MCM2-7 hexamers to form the pre-replicative complex. ATP hydrolysis by Cdc6 is required to remodel the MCM complex for bidirectional helicase activation at the G1/S transition, thereby ensuring that replication origins are licensed only once per cell cycle. As an E2F transcriptional target, Cdc6 serves as a link between mitogenic signaling and replication licensing, coordinates with cyclin-dependent kinases and Cdc7 for origin firing, and upholds checkpoints that prevent DNA re-replication. Following the S phase, Cdc6 is degraded through the ubiquitin-proteasome pathway to reset replication licensing. Dysregulation of Cdc6 drives oncogenesis, as its overexpression in cancers such as colorectal, lung, and cervical tumors enhances proliferation through interactions with cyclins and induces replication stress, while mutations can lead to genomic instability. Cdc6 is also involved in suppressing mitosis and activating cell cycle checkpoints.

References
https://pubmed.ncbi.nlm.nih.gov/22908236/ https://pubmed.ncbi.nlm.nih.gov/18048387/

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%