Cyclin-dependent kinase 9 Antibodies

Cyclin-dependent kinase 9 (CDK9)

Protein kinase involved in the regulation of transcription. Member of the cyclin-dependent kinase set (CDK9/cyclin-T) complex, also called positive transcription elongation factor b (P-TEFb), which eases the transition from abortive to productive elongation by phosphorylating the CTD (C-terminal domain) of the large subunit of RNA polymerase II (RNAP II) POLR2A, SUPT5H and RDBP.

Regulates cytokine inducible transcription networks by facilitating promoter recognition of target transcription factors (e.g.

Gene Information

Human
Gene Name:	CDK9
Uniprot:	P50750
Entrez:	1025

Family

Belongs to:
protein kinase superfamily

Alternative Names

C-2k; CDC2L4CTK1; CDC2-related kinase; Cell division cycle 2-like protein kinase 4; Cell division protein kinase 9; cyclin-dependent kinase 9 (CDC2-related kinase); cyclin-dependent kinase 9; EC 2.7.11; EC 2.7.11.22; EC 2.7.11.23; PITALRE; serine/threonine protein kinase PITALRE; Serine/threonine-protein kinase PITALRE; TAK

Molecular Weight

Mass (kDA):
42.778 kDA

Genomic Context

Human
Location:	9q34.11
Sequence:	9; NC_000009.12 (127786034..127790792)

Tissue Specificity

Ubiquitous.

Subcellular Localizations

Nucleus. Cytoplasm. Nucleus, PML body. Accumulates on chromatin in response to replication stress. Complexed with CCNT1 in nuclear speckles, but uncomplexed form in the cytoplasm. The translocation from nucleus to cytoplasm is XPO1/CRM1-dependent. Associates with PML body when acetylated.

Diseases

• Hiv Infections
• Immunologic Deficiency Syndromes
• Malignant Neoplasms
• Neoplasms
• Leukemia
• Hypertrophy
• Retinoblastoma
• Cardiac Hypertrophy
• Cell Transformation, Neoplastic
• Acquired Immunodeficiency Syndrome
• Carcinoma

• Malignant Paraganglionic Neoplasm
• Cytomegalovirus Infections
• Multiple Myeloma
• Lymphoid Leukemia
• Inflammation
• Chronic Lymphocytic Leukemia

Interacting Proteins

• ATR
• ATRIP
• CCNT1
• CDC37
• CLSPN

• FKBP5
• HEXIM1
• HSP90AA1
• HSP90AB1
• JMJD6

• LARP7
• PPP5C
• STAT3

Pathways

• Cell Cycle
• Localization
• Viral Replication
• Cell Death
• Cell Growth
• Viral Transcription
• Rna Interference
• Cell Division
• Hyperphosphorylation
• Chromatin Remodeling
• Cell Differentiation
• Translation
• Cell Proliferation

• Cell Cycle Arrest
• Induction Of Apoptosis
• S Phase
• Macrophage Differentiation
• Dna Repair
• Pathogenesis
• Methylation

PTMs

• Phosphorylation
• Acetylation
• Dephosphorylation
• Methylation

• Cleavage
• Ubiquitination
• Deamination
• Deacetylation

• Oxidation

Research Areas

• Cancer
• Cell Cycle and Replication
• Signal Transduction
• Virology, Bacteria and Parasites

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CDK9

Boster Bio Anti-Cyclin-Dependent Kinase 9 Marker

In this article, we'll look at the Boster Bio CDK9 Antibody and its Validation. We'll also go over its Applications and how it has been tested and validated. Boster Bio's Anti-Cyclin-dependent kinase 9 antibody is a reagent that reacts with human, mouse, and rat cells. This antibody can be used for research purposes. Find out more.

Boster Bio Anti-Cyclin-dependent kinase 9 CDK9 Marker

Boster Bio Anti-Cyclin-Dependent Kinase 9 (CDK9) Marker is a highly specific antibody for CDK9, a member of the Cdc2-like kinase family. CDK9 regulates cell differentiation and growth. Its pharmacological activity inhibits the growth of hormone-resistant and hormone-sensitive breast cancer cell lines.

The biological function of CDK9 and cyclin T1 is well-known. They regulate HEXIM1 and P-TEFb in the laboratory. They recruit SCF E3 Ubiquitin Ligases by their Cterminal PEST domain. But, polyubiquitination can lead to CDK9 degradation by proteasomes. Although polyubiquitination causes the enzyme to be destroyed, the concentration or DNA doesn't change. The level of protein is not affected in the same way as the kinases that regulate the cell cycle. It is unclear if the degrading of CDK9 has an effect on its function.

In addition to acting as a cell cycle regulator, CDK9 is also a cell cycle, CDK9 is also a member of the positive transcription elongation factor family of. It is a transcription regulator that promotes gene expression by recruiting target gene enhancers. This protein is involved in cell signaling through the 7SK snRNP complex that is composed of at least eight members. This complex interacts with NCOR1, HDAC3, PP2B and PPP1CA, which dephosphorylates Thr3.

CDK9 is a key transcription regulator and has been extensively utilized by cancer cells. It is believed to be an important driver of tumorigenesis. It is also linked to various forms of cancer, the majority of which utilize CDK9 for transcription. Its function is well-known, and many drugs that target CDK9 are currently in clinical trials.

The Boster Bio Anti-Cyclin-Dependent Kinase 9 CDK9 Marker is a highly sensitive tool for detection and quantification of CDK9 in various samples. The CDK9 Marker is used in different labs since 1998 and was designed for researchers to use in their experiments. In addition to being highly specific, it can be used to observe the activity of CDK in various cancer cell lines.

Various signaling pathways regulate CDK9 function and expression in cancer cells. Phosphorylation of HEXIM1 and Acetylation of Cyclin T1 are two main PTMs that liberate P-TEFb. Different post-translational modifications can also be utilized to control CDK9. JMJD6 is a phosphatase that demethylates the 5' end of 7SKRNA, also recruits this protein.

Applications

The CDK9 marker which is expressed in human cells, is associated with transcription extension. It is part of a complex which is connected to cyclin T which regulates gene transcription elongation as well as mRNA maturation. When activated, CDK9 phosphorylates the large subunit of RNAPII at CTD, a crucial step in maturing mRNA and anti-apoptotic gene expression. This pathway could be used as a potential drug target for malignant tumors.

The expression of CDK9 is associated with osteosarcoma, and could be a potential therapeutic target. Although the role of CDK9 is not fully understood but it does play crucial roles in the development of osteosarcoma cells. The progression of osteosarcoma is more rapid when osteosarcoma cells are overexpressed for CDK9. Additionally, CDK9 expression is linked with a better prognosis in osteosarcoma patients.

Similar to panc89 cells, CDK9 activity is essential for survival. CDK9 activity also enhances the expression anti-apoptotic protein. These findings have led the identification of CDK9 as an effective therapeutic target in cancer research. The CDK9 marker is a promising method for diagnosis and treatment and regenerative medicine. This marker can be used to detect patients suffering from cancers on both sides of the colon.

IHC and Cell Signaling Technology assays were used to determine the expression level of CDK9. The paraffin-embedded slides had to be baked at 60 degrees Celsius for one hour , before being rehydrated with graded alcohol, and then blocked with normal goat serum for 1 hour. After blocking for an hour after which the slides were baked with paraffin-embedded slides. The slides were again rehydrated using graded ethanol, and blocked with normal goat serum for 1 hour. CDK9 expression was then confirmed by using an CDK9 immunostain in bovine serum-PBS.

Specific siRNA was used to suppress CDK9 in osteosarcoma cells. U2OS and KHOS cells were grown at 2x each in 12-well plates. Increasing concentrations of CDK9 siRNA were transfected using the RNAiMax lipofectamine reagent or with an unspecific control. The cells were then analysed for MTT levels and protein levels to determine the degree of cell growth.

CDK9 is correlated with genes that regulate the immune cell's migration and exhaustion. It is associated with the expression of genes NFATC1, ACKR3, NFAT5. It has also been shown to be associated with the expression C10orf54 V set immunoregulatory receptor. TPM is the abbreviation for transcripts per million. This marker has numerous applications in clinical and research. It is currently used in a variety of research settings, including immunohistochemistry.

Validation

Recent research has confirmed the CDK9 marker in Boster Bio's Boster Bio anti-Cdk9 antibodies by using antibodies to human CDK9. Researchers examined the effect of CDK9 on human ovarian cancer cell growth using a 3-D (3D) cell culture assay. Cell lines were grown in 24 well VitroGel 3D cell culture plates that contained two x 104 cells per well. Different cultures of cells were added to the hydrogel cover each well.

The level of expression of CDK9 was determined by using an Immunohistochemistry Protocol developed by Cell Signaling Technology. Then equal amounts of human CDK9 antibody were injected into the array and incubated for overnight at 4°C. SignalStain DAB and SignalStain Boost were used to detect the binding of antibodies to the array. Finally, the slides were counter-stained using Hematoxylin QS and mounted with VectaMount AQ.

In addition to being an independent marker for prognosis, CDK9 was also associated with poorer patient outcomes. Patients with low levels CDK9 had a significantly lower outlook than those with higher levels. Additionally, higher CDK9 expression in ovarian cancer tissues correlated with a lower survival rate for patients, when compared with those with high levels of CDK9.

CDK9 knockdown inhibited cell proliferation in ovarian cancer cells. Transfection with synthetic CDK9 siRNA resulted in a decrease of cell proliferation, but there was no change in general expression levels. The effect was also observed in ovarian cancer cell line IGROV-1. These results confirm that CDK9 is a significant element in determining the ovarian cancer cells' proliferation. This means that it is able to accurately detect cancerous ovarian cells in an environment of clinical.

It does not just reduce the growth of ovarian carcinoma cells but also stops their migration. CDK9 inhibition reduces cell growth and the possibility of clonogenicity. Therefore, this marker has significant clinical utility. Boster bio's CDK9 inhibitor LDC067 blocks the growth and spread of cancerous ovarian cells. It prolongs the survival of patients suffering from leukemia, and also blocks their anti-tumor response.

CDK9 phosphorylates the CTD during transcription in initiation and elongation. CDK9 plays a key role in various types of cancer such as prostate, cervical, breast, and Melanoma. However, the connection between CDK9 expression and prognosis remains unclear. In the end, this gene could serve as a potential target for cancer therapy. These findings are not conclusive at the moment. These findings can provide useful information regarding the role of CDK9 within different types of cancer.