DNA damage repair markers

Unrepaired DNA damage leads to mutagenesis or cell death.

DNA mutations are a known factor in the tumorigenesis of many cancer types including colon and skin cancer, leukemia, lymphoma, and breast or ovarian cancer.

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The accumulation of DNA damage in myocytes or neurons can result in degenerative diseases (1). The human brain consumes 20% of the body’s entire oxygen intake to generate sufficient energy to maintain its proper functioning. Since ROS (Reactive Oxygen Species) are a natural side-product of the pathways of this energy production, they can be easily accumulated in the brain and induce DNA damage.

Every day, cells are exposed to a broad range of DNA-damaging factors (2). As a safeguard for genome stability, they have developed many repair pathways, especially for damage from oxidation, hydrolysis, dimerization of DNA-bases, and single or double strand DNA breaks (Figure 1).

  

Figure 1. Overview of DNA damage-specific repair pathways. Response mechanisms: Direct reversal, MMR (MisMatch Repair), BER (Base Excision Repair), NER (Nucleotide Excision Repair), HR (Homologous Recombination), MMEJ (Microhomology-Mediated End Joining), and NHEJ (Non-Homologous End Joining).

Figure 2. Immunohistochemical analysis of paraffin-embedded human small intestine tissue slide using 60277-1-Ig ( CHK1 Antibody) at dilution of 1:50 (under 10x lens).

Climate change and increased environmental pollution are extending DNA-damaging factors. It is therefore important to understand the DNA damage repair mechanisms. Tomas Lindahl, Paul Modrich, and Aziz Sancarwere pioneers in discovering the molecular basis of DNA damage repair pathways (2015, with the Nobel Prize in Chemistry).

Figure 3. WB result of CDC25C antibody (16485-1-AP; 1:4000; incubated at room temperature for 1.5 hours) with sh-Control and sh-CDC25C transfected HeLa cells.

Figure 4. WB result of NBS1 antibody (55025-1-AP; 1:2000; incubated at room temperature for 1.5 hours) with sh-Control and sh-NBS1 transfected HeLa cells

DNA damage repair markers

DNA damage marker	Type	Cat. No.	Damage type/ Repair mechanism
ATM	Rabbit	27156-1-AP	DSB
ATR	Rabbit	19787-1-AP	SSB
ATRIP	Rabbit	11327-1-AP	SSB
Cdc25A	Rabbit	55031-1-AP	SSB, DSB
Cdc25B	Rabbit	10644-1-AP	SSB, DSB
Cdc25C	Rabbit, Mouse	16485-1-AP  (Figure 3) ; 66912-1-Ig	SSB, DSB
Chk1	Rabbit, Mouse	25667-1-AP; 60277-1-Ig  (Figure 2)	SSB
Chk2	Rabbit	13954-1-AP	DSB
DDB1	Rabbit, Mouse	11380-1-AP; 66010-1-Ig	SSB/ NER
DDB2	Rabbit	10431-1-AP	SSB/ NER
Fen1	Rabbit	14768-1-AP	DSB/ MMEJ
H2AX	Rabbit	10856-1-AP	DSB
Ku70	Rabbit, Mouse	10723-1-AP; 66607-1-Ig	DSB/ NHEJ
Ku80	Rabbit, Mouse	16389-1-AP; 66546-1-Ig	DSB/ NHEJ
Mre11	Rabbit	10744-1-AP	DSB/ HR
Nbs1	Rabbit	55025-1-AP  (Figure 4)	DSB/ HR
PCNA	Rabbit, Mouse	10205-1-AP; 60097-1-Ig	SSB/ NER
POLD1	Rabbit	15646-1-AP	SSB
POLD2	Rabbit	10288-1-AP	SSB
POLD3	Rabbit	21935-1-AP	SSB
POLD4	Rabbit	26209-1-AP	SSB
POLE3	Rabbit	15278-1-AP	SSB
POLK	Rabbit	14455-1-AP	SSB
Rad1	Rabbit	11726-2-AP	SSB
Rad51	Rabbit, Mouse	14961-1-AP; 67024-1-Ig	DSB/ HR
RFC2	Rabbit	10410-1-AP	SSB/ NER
RFC3	Rabbit	11814-1-AP	SSB/ NER
RFC4	Rabbit	10806-1-AP	SSB/ NER
RFC5	Rabbit	10385-1-AP	SSB/ NER
RPA1	Rabbit	12448-1-AP	SSB, DSB/ HR
RPA2	Rabbit	10412-1-AP	SSB, DSB/ HR
RPA3	Rabbit	10692-1-AP	SSB, DSB/ HR
RPA4	Rabbit	18144-1-AP	SSB, DSB/ HR

Loading control antibodies

GAPDH Antibody

Catalog no.: 60004-1-Ig

GAPDH is commonly used as a protein loading control in western blot due to its consistently high expression in most cell types. This enzyme participates in several cellular events such as glycolysis, DNA repair, and apoptosis.

Proteintech monoclonal GAPDH antibodies are raised against a whole-protein antigen of human origin and have over 4,960 citations.

Beta Actin Antibody (KD/KO validated)

Catalog no.: 66009-1-Ig 

Beta-actin is usually used as a loading control due to its broad and consistent expression across all eukaryotic cell types and the fact that expression levels of this protein are not affected by most experimental treatments.

66009-1-Ig has been cited in over 2,460 publications and has wide species reactivity.

Homologous Recombination (HR)
Table 1. List of available antibodies against DNA damage markers and the DNA damage pathway(s)

Double Strand Breaks (DSB)

Microhomology-Mediated End Joining (MMEJ)

Nucleotide Excision Repair (NER)

Non-Homologous End Joining (NHEJ)

Single Strand Breaks (SSB)

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References

1. Stein and Toiber (2017) “DNA damage and neurodegeneration: the unusual suspect”.

2. Lindahl and Barnes (2000) “Repair of endogenous DNA damage“.