Product: CDK1/CDC2 Antibody
Catalog: DF6024
Description: Rabbit polyclonal antibody to CDK1/CDC2
Application: WB IHC IF/ICC
Cited expt.: WB, IHC
Reactivity: Human, Mouse, Rat
Mol.Wt.: 34kDa; 34kD(Calculated).
Uniprot: P06493
RRID: AB_2837999

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 100ul $280 In stock
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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Clonality:
Polyclonal
Specificity:
CDK1/CDC2 Antibody detects endogenous levels of total CDK1/CDC2.
RRID:
AB_2837999
Cite Format: Affinity Biosciences Cat# DF6024, RRID:AB_2837999.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

Cdc 2; Cdc2; CDC28A; CDK 1; CDK1; CDK1_HUMAN; CDKN1; CELL CYCLE CONTROLLER CDC2; Cell division control protein 2; Cell division control protein 2 homolog; Cell division cycle 2 G1 to S and G2 to M; Cell division protein kinase 1; Cell Divsion Cycle 2 Protein; Cyclin Dependent Kinase 1; Cyclin-dependent kinase 1; DKFZp686L20222; MGC111195; p34 Cdk1; p34 protein kinase; P34CDC2;

Immunogens

Immunogen:

A synthesized peptide derived from human CDK1/CDC2, corresponding to a region within the internal amino acids.

Uniprot:
Gene(ID):
Expression:
P06493 CDK1_HUMAN:

Isoform 2 is found in breast cancer tissues.

Description:
The entry of eukaryotic cells into mitosis is regulated by cdc2 kinase activation, a process controlled at several steps including cyclin binding and phosphorylation of cdc2 at Thr161 (1). However, the critical regulatory step in activating cdc2 during progression into mitosis appears to be dephosphorylation of cdc2 at Thr14 and Tyr15 (2). Phosphorylation at Thr14 and Tyr15, resulting in inhibition of cdc2, can be carried out by Wee1 and Myt1 protein kinases (3,4). The cdc25 phosphatase may be responsible for removal of phosphates at Thr14 and Tyr15 and subsequent activation of cdc2 (1,5).
Sequence:
MEDYTKIEKIGEGTYGVVYKGRHKTTGQVVAMKKIRLESEEEGVPSTAIREISLLKELRHPNIVSLQDVLMQDSRLYLIFEFLSMDLKKYLDSIPPGQYMDSSLVKSYLYQILQGIVFCHSRRVLHRDLKPQNLLIDDKGTIKLADFGLARAFGIPIRVYTHEVVTLWYRSPEVLLGSARYSTPVDIWSIGTIFAELATKKPLFHGDSEIDQLFRIFRALGTPNNEVWPEVESLQDYKNTFPKWKPGSLASHVKNLDENGLDLLSKMLIYDPAKRISGKMALNHPYFNDLDNQIKKM

Research Backgrounds

Function:

Plays a key role in the control of the eukaryotic cell cycle by modulating the centrosome cycle as well as mitotic onset; promotes G2-M transition, and regulates G1 progress and G1-S transition via association with multiple interphase cyclins. Required in higher cells for entry into S-phase and mitosis. Phosphorylates PARVA/actopaxin, APC, AMPH, APC, BARD1, Bcl-xL/BCL2L1, BRCA2, CALD1, CASP8, CDC7, CDC20, CDC25A, CDC25C, CC2D1A, CENPA, CSNK2 proteins/CKII, FZR1/CDH1, CDK7, CEBPB, CHAMP1, DMD/dystrophin, EEF1 proteins/EF-1, EZH2, KIF11/EG5, EGFR, FANCG, FOS, GFAP, GOLGA2/GM130, GRASP1, UBE2A/hHR6A, HIST1H1 proteins/histone H1, HMGA1, HIVEP3/KRC, LMNA, LMNB, LMNC, LBR, LATS1, MAP1B, MAP4, MARCKS, MCM2, MCM4, MKLP1, MYB, NEFH, NFIC, NPC/nuclear pore complex, PITPNM1/NIR2, NPM1, NCL, NUCKS1, NPM1/numatrin, ORC1, PRKAR2A, EEF1E1/p18, EIF3F/p47, p53/TP53, NONO/p54NRB, PAPOLA, PLEC/plectin, RB1, TPPP, UL40/R2, RAB4A, RAP1GAP, RCC1, RPS6KB1/S6K1, KHDRBS1/SAM68, ESPL1, SKI, BIRC5/survivin, STIP1, TEX14, beta-tubulins, MAPT/TAU, NEDD1, VIM/vimentin, TK1, FOXO1, RUNX1/AML1, SAMHD1, SIRT2 and RUNX2. CDK1/CDC2-cyclin-B controls pronuclear union in interphase fertilized eggs. Essential for early stages of embryonic development. During G2 and early mitosis, CDC25A/B/C-mediated dephosphorylation activates CDK1/cyclin complexes which phosphorylate several substrates that trigger at least centrosome separation, Golgi dynamics, nuclear envelope breakdown and chromosome condensation. Once chromosomes are condensed and aligned at the metaphase plate, CDK1 activity is switched off by WEE1- and PKMYT1-mediated phosphorylation to allow sister chromatid separation, chromosome decondensation, reformation of the nuclear envelope and cytokinesis. Inactivated by PKR/EIF2AK2- and WEE1-mediated phosphorylation upon DNA damage to stop cell cycle and genome replication at the G2 checkpoint thus facilitating DNA repair. Reactivated after successful DNA repair through WIP1-dependent signaling leading to CDC25A/B/C-mediated dephosphorylation and restoring cell cycle progression. In proliferating cells, CDK1-mediated FOXO1 phosphorylation at the G2-M phase represses FOXO1 interaction with 14-3-3 proteins and thereby promotes FOXO1 nuclear accumulation and transcription factor activity, leading to cell death of postmitotic neurons. The phosphorylation of beta-tubulins regulates microtubule dynamics during mitosis. NEDD1 phosphorylation promotes PLK1-mediated NEDD1 phosphorylation and subsequent targeting of the gamma-tubulin ring complex (gTuRC) to the centrosome, an important step for spindle formation. In addition, CC2D1A phosphorylation regulates CC2D1A spindle pole localization and association with SCC1/RAD21 and centriole cohesion during mitosis. The phosphorylation of Bcl-xL/BCL2L1 after prolongated G2 arrest upon DNA damage triggers apoptosis. In contrast, CASP8 phosphorylation during mitosis prevents its activation by proteolysis and subsequent apoptosis. This phosphorylation occurs in cancer cell lines, as well as in primary breast tissues and lymphocytes. EZH2 phosphorylation promotes H3K27me3 maintenance and epigenetic gene silencing. CALD1 phosphorylation promotes Schwann cell migration during peripheral nerve regeneration. CDK1-cyclin-B complex phosphorylates NCKAP5L and mediates its dissociation from centrosomes during mitosis. Regulates the amplitude of the cyclic expression of the core clock gene ARNTL/BMAL1 by phosphorylating its transcriptional repressor NR1D1, and this phosphorylation is necessary for SCF(FBXW7)-mediated ubiquitination and proteasomal degradation of NR1D1.

(Microbial infection) Acts as a receptor for hepatitis C virus (HCV) in hepatocytes and facilitates its cell entry.

PTMs:

Phosphorylation at Thr-161 by CAK/CDK7 activates kinase activity. Phosphorylation at Thr-14 and Tyr-15 by PKMYT1 prevents nuclear translocation. Phosphorylation at Tyr-15 by WEE1 and WEE2 inhibits the protein kinase activity and acts as a negative regulator of entry into mitosis (G2 to M transition). Phosphorylation by PKMYT1 and WEE1 takes place during mitosis to keep CDK1-cyclin-B complexes inactive until the end of G2. By the end of G2, PKMYT1 and WEE1 are inactivated, but CDC25A and CDC25B are activated. Dephosphorylation by active CDC25A and CDC25B at Thr-14 and Tyr-15, leads to CDK1 activation at the G2-M transition. Phosphorylation at Tyr-15 by WEE2 during oogenesis is required to maintain meiotic arrest in oocytes during the germinal vesicle (GV) stage, a long period of quiescence at dictyate prophase I, leading to prevent meiotic reentry. Phosphorylation by WEE2 is also required for metaphase II exit during egg activation to ensure exit from meiosis in oocytes and promote pronuclear formation. Phosphorylated at Tyr-4 by PKR/EIF2AK2 upon genotoxic stress. This phosphorylation triggers CDK1 polyubiquitination and subsequent proteolysis, thus leading to G2 arrest. In response to UV irradiation, phosphorylation at Tyr-15 by PRKCD activates the G2/M DNA damage checkpoint.

Polyubiquitinated upon genotoxic stress.

Subcellular Location:

Nucleus. Cytoplasm. Mitochondrion. Cytoplasm>Cytoskeleton>Microtubule organizing center>Centrosome. Cytoplasm>Cytoskeleton>Spindle.
Note: Cytoplasmic during the interphase. Colocalizes with SIRT2 on centrosome during prophase and on splindle fibers during metaphase of the mitotic cell cycle. Reversibly translocated from cytoplasm to nucleus when phosphorylated before G2-M transition when associated with cyclin-B1. Accumulates in mitochondria in G2-arrested cells upon DNA-damage.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Isoform 2 is found in breast cancer tissues.

Family&Domains:

Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily.

Research Fields

· Cellular Processes > Cell growth and death > Cell cycle.   (View pathway)

· Cellular Processes > Cell growth and death > Oocyte meiosis.   (View pathway)

· Cellular Processes > Cell growth and death > p53 signaling pathway.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Gap junction.   (View pathway)

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Organismal Systems > Endocrine system > Progesterone-mediated oocyte maturation.

References

1). Effects of iron oxide nanoparticles as T2-MRI contrast agents on reproductive system in male mice. Journal of Nanobiotechnology, 2022 [IF=10.2]

Application: WB    Species: Mouse    Sample:

Fig. 5 The evaluation of hormones and the effects on testes in male ICR mice with intravenous injection of IONPs. a–c The levels of hormones that were highly correlated with spermatogenesis in ICR mice at 1, 3, 7, 14 and 28 days after intravenous injection of IONPs, including FSH (a), LH (b) and testosterone (c). d–f The photo of testes (d), unilateral testicular index-changing curves (e) and accumulation of Fe ions in testes evaluated by ICP-AES (f). Data were expressed as the Mean ± S.E.M., n = 5. g, h CDC2 and Cyclin B1 protein levels detected by western blotting (g) and further quantified by ImageJ software (h) in male ICR mice at 1 day after intravenous injection of IONPs with various concentrations. Data were representative of three independent experiments, β-actin served as a loading control. i Histopathological examination of testes in ICR mice at 1, 3, 7, 14 and 28 days after intravenous injection of IONPs with various concentrations. Abnormal cells were indicated by black arrows. Scale bar, 100 μm. j, k Evaluation of N-cadherin (j) and Occludin (k) by immunohistological staining. Positive staining was indicated by red arrows. Scale bar, 100 μm

2). Efects of iron oxide nanoparticles as T2-MRI contrast agents on reproductive system in male mice. Journal of Nanobiotechnology, 2022 [IF=10.2]

3). Muscone restores anoikis sensitivity in TMZ-resistant glioblastoma cells by suppressing TOP2A via the EGFR/Integrin β1/FAK signaling pathway. Phytomedicine : international journal of phytotherapy and phytopharmacology, 2024 (PubMed: 38723526) [IF=6.7]

4). Design and synthesis of isatin derivative payloaded peptide-drug conjugate as tubulin inhibitor against colorectal cancer. European journal of medicinal chemistry, 2025 (PubMed: 39818012) [IF=6.0]

5). Primary microcephaly gene CENPE is a novel biomarker and potential therapeutic target for non-WNT/non-SHH medulloblastoma. Frontiers in Immunology, 2023 (PubMed: 37593739) [IF=5.7]

Application: WB    Species: Human    Sample:

Figure 9 CENPE regulates the cell cycle and p53 pathway of non-WNT/non-SHH MB. (A–E) Western blot showed that the protein level of CENPE, P53, P21 and CDK1 by the knockdown of CENPE (mean ± SD, n = 3). (F–H) Flow cytometry was used to detect the cell cycle (mean ± SD, n = 3).

6). FGF21 attenuates pulmonary arterial hypertension via downregulation of miR‐130, which targets PPARγ. Journal of Cellular and Molecular Medicine, 2022 (PubMed: 34989130) [IF=5.3]

Application: WB    Species: Mice    Sample:

FIGURE 3 MiR‐130 increases hypoxia‐induced PASMC proliferation and migration by regulating PPARγ expression. (A–C) Western blotting for proliferating cell nuclear antigen (PCNA), cyclin‐dependent kinase 1 (CDK1) and cyclin D1 in Nor, Hyp, Hyp+miR‐130 inhibitor and Hyp+miR‐130 inhibitor+siPPARγ groups, β‐actin was used as a loading control (n = 4). (D–F) qRT‐PCR was used to detect mRNA expression of PCNA, CDK1 and cyclin D1 in each group. The mRNA level is normalized to β‐actin by the 2−ΔCt method before comparative analysis (n = 4). (g) CCK‐8 assay (n = 5) and (H) BrdU incorporation study (n = 6) were used to evaluate cell viability. (I) Cell migration was determined by Transwell assays at 24 h (n = 4; ×100; scale bars indicate 200 µm). (J) Cell migration was determined by wound‐healing assays at 0 and 48 h (n = 3) (×200; scale bars indicate 100 µm). Data are presented as the mean ± SD. *p < 0.05, **p < 0.01

7). Ochratoxin A induces cytotoxicity through ROS-mediated endoplasmic reticulum stress pathway in human gastric epithelium cells. TOXICOLOGY, 2022 (PubMed: 36058351) [IF=4.8]

8). Novel circRNA_0071196/miRNA‑19b‑3p/CIT axis is associated with proliferation and migration of bladder cancer. INTERNATIONAL JOURNAL OF ONCOLOGY, 2020 (PubMed: 32705161) [IF=4.5]

Application: WB    Species: Human    Sample: 5637 cells

Figure 11 Molecular basis of CIT action in BCa cells. Expression levels of p53, MLC2, CDK1, MDM2, CCND1 and ROCK1 mRNA (A) and protein (B and C) in sh-CIT and sh-Control-transfected 5637 cells. *P

9). Circ_0011385 knockdown inhibits cell proliferation, migration and invasion, whereas promotes cell apoptosis by regulating miR-330-3p/MYO6 axis in colorectal cancer. Biomedical Journal, 2023 (PubMed: 35091088) [IF=4.1]

Application: WB    Species: Human    Sample: HCT116 and SW480 cells

Fig. 4. Circ_0011385 silencing suppressed CRC development by interacting with miR-330-3p. (A and B) The effect of miR-330-3p inhibitor on miR-330-3p expression was determined by qRT-PCR in HCT116 and SW480 cells. (C–E) The impacts between circ_0011385 silencing and miR-330-3p inhibitor on the proliferation of HCT116 and SW480 cells were unveiled by MTT assay and cell colony formation assay. (F, I and J) Flow cytometry analysis was utilized to illustrate the effects between circ_0011385 silencing and miR-330-3p inhibitor on the apoptosis and cell cycle of HCT116 and SW480 cells. (G and H) Wound-healing and transwell assays were performed to reveal the influences between circ_0011385 absence and miR-330-3p inhibitor on the migration and invasion of HCT116 and SW480 cells, respectively. (K and L) Western blot assay was conducted to determine the influences between circ_0011385 downregulation and miR-330-3p inhibitor on the protein expression of CDK1 and Cyclin D1 in HCT116 and SW480 cells.

10). Transcriptome analysis reveals the anticancer effects of fenbendazole on ovarian cancer: an in vitro and in vivo study. BMC cancer, 2024 (PubMed: 39736624) [IF=3.8]

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