CDK16 Antibodies

Cyclin-dependent kinase 16 (CDK16)

Protein kinase that plays a role in vesicle-mediated transportation processes and exocytosis. Regulates GH1 release by brain neurons.

Phosphorylates NSF, and thereby regulates NSF oligomerization. Required for normal spermatogenesis.

Gene Information

Human
Gene Name:	CDK16
Uniprot:	Q00536
Entrez:	5127

Family

Belongs to:
protein kinase superfamily

Alternative Names

Cell division protein kinase 16; cyclin-dependent kinase 16; EC 2.7.11; EC 2.7.11.22; FLJ16665; PCTAIRE protein kinase 1; PCTAIRE; PCTAIRE1; PCTAIRE-motif protein kinase 1; PCTGAIRE; PCTK1Serine/threonine-protein kinase PCTAIRE-1

Molecular Weight

Mass (kDA):
55.716 kDA

Genomic Context

Human
Location:	Xp11.3
Sequence:	X; NC_000023.11 (47217881..47229997)

Tissue Specificity

Detected in pancreas islets (at protein level). Detected in brain and pancreas.

Subcellular Localizations

Cytoplasm. Cytoplasmic vesicle, secretory vesicle. Cell membrane; Peripheral membrane protein; Cytoplasmic side. Cell junction, synapse, synaptosome. Colocalizes with insulin in pancreas islets. Recruited to the cell membrane by CCNY.

Diseases

• Male Infertility
• Nervousness
• Infertility

Interacting Proteins

• APPBP2
• CCNYL1
• SEC23A
• ZBTB14

Pathways

• Spermatogenesis
• Neuron Migration
• Brain Development

PTMs

• Phosphorylation

• Myristoylation

Research Areas

• Cell Cycle and Replication

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CDK16

Boster Bio - Best Uses Of The CDK16 Marker

A biography of Steven Boster, Historie of the CDK16 Marker, is highly recommended for all scientists. It can be found online at the Boster Bio section. This biography can be used by all scientists worldwide. This article will focus on the biography and uses of the CDK16 mark. Amazon also offers the Historie about the CDK16 Marker. This gene-marker offers many benefits in your research.

Historie

The CDK16 gene is a key player in epithelial-mesenchymal transition, a primary step in the invasion of cancer cells. Many studies have linked the increased expression of CDK16 with metastasis development and HCC. Moreover, in silico analyses revealed that downregulation of CDK16 suppressed tumor cell migration and invasion. Moreover, overexpression of CDK16 induced the appearance of a mesenchymal-like morphological feature in the L02 cell line.

CDK16 is a common upregulated protein in HCC. E2F1 is an important upstream regulator of this protein. ChIP assays and luciferase reporter analysis confirmed the positive correlation between E2F1 and CDK16. CDK16, E2F1 and TCGA cohorts were associated with bilateral regulation in cell fate. This correlation has also been confirmed by gene expression studies in human HCC.

CDK16 promotes cell proliferation and inhibits the death of cells. It regulates GSK-3b activity, which is a key regulator of tumor growth and EMT. CDK16, with its multiple activating mechanisms, could be a target for HCC. It is believed to be an indicator of the disease. This discovery provides valuable tools for diagnosing HCC and determining its prognosis.

CDKs/CDKIs play a key role in the brain's growth. They play many roles in embryonic growth, with a particular focus on the brain, pancreas and gonadal. CDK16/CDKIs can also be linked to Parkinson's Disease and Alzheimer's. If your CDK16 gene expression is low, this gene is likely to be down-regulated.

MicroRNAs play an important role in the regulation of oncogenes after transcription. Three miRNA targets have been identified in CDK16's 3'UTR. One of these, miR125b-5p, is a miRNA target that inhibits EMT. Therefore, the loss of miR125b-5p in humans may cause CDK16 to be upregulated in HCC.

Historie on the CDK16 Marker

CDK16 belongs to the essential family of cyclindependent-kinases. These proteins are important in the regulation and integration of extracellular as well intracellular signals. CDK16 is also involved in spermatogenesis (neurogenesis) and spermatogenesis (spermatogenesis). However, it remains to be determined its exact role as a neuronal developmental and migration regulator.

CDK16 is able to interact with CCNY through an unexpected mechanism. The key factor in gene expression regulation is the novel interaction between CDK16 & CCNY. CDK16 may be required for CCNY protein phosphorylation, according to some theories. It is still not clear what role CCNY plays in the interaction between CDK16 and cyclin-related gene genes. However, this is a significant step in our understanding of how CDK16 interacts CCNY.

It is not clear why CDK16 regulates cells growth. However, CDK16 expression is a strong indicator for functions that are not directly related to proliferation. Mutants of PCT-1 had misbalanced intracellular vesicle transport. This suggests that PCTKs may be involved in the regulation of intracellular vesicle transportation. They have been implicated also in neurite outgrowth.

The embryonic development of mice lacking CDK16 was normal, but the spermatozoa were abnormal. CDK16-deficient mice showed abnormalities in spermatozoa. These included an elongated annulus. They were also bent and lacked motility. This shows that CDK16 is essential for spermatogenesis. CDK16 plays an essential role in embryonic and developmental development.

In HCC, CDK16 is frequently upregulated. It is cytoplasm-localized. It increases throughout the course of the illness. The highest CDK16 expression was found in PVTT positive HCCs. It was associated with several clinical pathological features, poor patient outcomes, and poor survival and recurrence. These results suggest CDK16 as a therapeutic target in HCC.

Although Cdks are not essential for brain development, they play crucial roles in the development neurons. Cdk1 may be essential for embryonic growth, but it doesn't appear to play an important role in the development of neurons. However, the loss of this gene could contribute to the upregulation of CDK16. Human HCC has miR125b-5p which inhibits EMT. This may lead to CDK16 being upregulated.