KIF2C Antibodies

Kinesin-like protein KIF2C (KIF2C)

In complex with KIF18B, constitutes the significant microtubule plus-end depolymerizing activity in mitotic cells (PubMed:21820309). Regulates the turnover of microtubules in the kinetochore and functions in chromosome segregation during mitosis (PubMed:19060894).

Plays a role in chromosome congression and is required for the lateral to end-on conversion of the chromosome- microtubule attachment (PubMed:23891108). .

Gene Information

Human
Gene Name:	KIF2C
Uniprot:	Q99661
Entrez:	11004

Family

Belongs to:
TRAFAC class myosin-kinesin ATPase superfamily

Alternative Names

kinesin family member 2C; kinesin-like 6 (mitotic centromere-associated kinesin); Kinesin-like protein 6; kinesin-like protein KIF2C; MCAKKNSL6kinesin-like 6; Mitotic centromere-associated kinesin

Molecular Weight

Mass (kDA):
81.313 kDA

Genomic Context

Human
Location:	1p34.1
Sequence:	1; NC_000001.11 (44739704..44767767)

Tissue Specificity

Expressed at high levels in thymus and testis, at low levels in small intestine, the mucosal lining of colon, and placenta, and at very low levels in spleen and ovary; expression is not detected in prostate, peripheral blood Leukocytes, heart, brain, lung, liver, skeletal muscle, kidney or pancreas. Isoform 2 is testis-specific.

Subcellular Localizations

Cytoplasm, cytoskeleton. Nucleus. Chromosome, centromere. Chromosome, centromere, kinetochore. Associates with the microtubule network at the growing distal tip (the plus-end) of microtubules, probably through interaction with MTUS2/TIP150 and MAPRE1 (By similarity). Association with microtubule plus ends is also mediated by interaction with KIF18B. Centromeric localization requires the presence of BUB1 and SGO2.

Diseases

• Malignant Neoplasms
• Neoplasms
• Malignant Neoplasm Of Breast
• Aneuploidy
• Mammary Neoplasms
• Neoplasm Metastasis
• Carcinoma
• Malignant Paraganglionic Neoplasm
• Cell Transformation, Neoplastic
• Metastatic Malignant Neoplasm To The Lymph Node
• Genomic Instability
• Colorectal Neoplasms
• Carcinogenesis

• Colorectal Cancer
• Cell Invasion
• Lymphatic Metastasis
• Malignant Neoplasm Of Stomach
• Leukemia
• Cholangiocarcinoma
• Acquired Immunodeficiency Syndrome

Interacting Proteins

• MAPRE1
• MTUS2

Pathways

• Mitosis
• Chromosome Segregation
• Spindle Assembly
• Localization
• Cell Cycle
• Anaphase
• Metaphase
• Cell Division
• Microtubule Depolymerization
• Interphase
• Cytokinesis
• Prophase
• Meiosis

• Rna Interference
• S Phase
• Transport
• Microtubule Nucleation
• Meiosis I
• Spindle Assembly Checkpoint
• Microtubule Polymerization

PTMs

• Phosphorylation
• Cleavage

• Methylation
• Dephosphorylation

Research Areas

• Cancer
• Cell Biology
• Cellular Markers
• DNA Repair

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/KIF2C

Best Uses Of The KIF2C Marker

This article will provide a basic understanding of KIF2C's functions, the gene that encodes the Cytokine kappa A. Additionally, you will learn how other markers of this gene are used, such as KIF4A, KIF18B. These markers regulate the activity of many enzymes including kinase.

KIF2C

KIF2C is a protein found in many types of tumors. Numerous studies have been done on this protein's role in cancer development and progression. It has been shown to predict the outcome of many types of cancer. KIF2C's co-expression network analysis suggested that this protein could be a new prognostic marker for the diagnosis of gliomas. The protein induced frequent T cell responses in colorectal Cancer.

KIF2C regulates the depolymerization MT protein, which is involved in synaptic flexibility. It also helps control the dynamics of microtubules in dendritic shafts. These results suggest that KIF2C plays a role in the regulation of dendritic spine dynamics. Additional studies are required to fully understand the mechanism behind KIF2C action within dendrites. Moreover, additional studies must address the possibility that KIF2C may leave the spines during synaptic activity, and the dynamics of MT invasion in dendrites.

KIF4A

Boster Bio Anti-KIF4A antibody is available for Western blot and ELISA. It is stored at -20degC for a year and reacts with Human. It is also available in liquid form in PBS. You can also buy blocking protein at a price that depends on how long the immunogen is. For more information, please refer to the Boster Bio article.

The mRNA expression levels of eight KIFs were significantly higher in HCC than in normal liver tissues. Moreover, downregulating one or more of them significantly decreased the proliferation of liver cancer cells in vitro. These proteins could serve as therapeutic targets in HCC. However, there are some limitations to this use. Although there is a lot research on KIFs in cancer, only a few studies have been conducted.

KIF10

KIF2C's physiological role is still unknown. The protein is involved in synaptic plasticity, cognition, and dynamic microtubule invasion of dendritic spines. This article will explore these roles and provide insight into how KIF2C can be used for neurological research. The article was peer reviewed by three scientists, including Anna Akhmanova the Senior Editor for Biochemistry and Molecular Biology. Yu-Tian Wang, Reviewing editor, agreed to identify him as an expert in the subject. The Reviewing Editor wrote a letter for the author to facilitate revision of the manuscript.

The KIF2C protein is essential for synaptic plasticity in the hippocampal neurons. The hippocampus could suffer from a deficiency in this protein, which may lead to a reduction in the basal function and activity of AMPARs. Although further studies are needed to determine the exact role of KIF2C, the results presented here are impressive. The KIF2C genome is essential for brain growth.

KIF18B

It has been proven that tumor samples expressing KIF18B correlate with PTEN gene mutation status. KIF18B expression is higher in mutant PTENPCa cancers than in wildtype PTENPCa. KIF18B expression was associated with biochemical treatment recurrence, tumor volume and Gleason score.

To perform the experiments, total RNA was isolated from cells using TRIzol. The optical density at 260-280 was used for determining the purity of total RNA. The FastKing RT Kit, PCR Thermal Cycler Dice were used to synthesize cDNA. The 2-DDCT method was used to calculate relative gene expression. Once the results of the experiment had been confirmed, the samples were processed to allow for further use.

It was interesting to note that chemotherapy patients who were not able to knock down KIF18B in their tumor cells were not more likely to survive. Radio and chemotherapy use different pathways to cause DNA damage. Ionizing radiation causes two-strand breaks while many of the chemotherapeutic agents cause damage through indirect mechanisms. In addition, KIF18B functional enrichment was associated with nucleotide excision repair (NER), a crucial component in DDR.

KIF20A

KIF2C, a key regulator of cell motility & proliferation, has been linked with many biological activities. It was recently identified in hepatocellular carcinoma as a target for Wnt/b–catenin and the mTORC1 signaling. KIF2C expression can be negatively regulated by miR-325-3p. It is also a key player in promoting cell motility. Recent bioinformatics analysis found that KIF2C levels are associated with poor outcomes in breast-cancer. This suggests that KIF2C could be a prognosis biomarker for this disease.

Interestingly, the expression of KIF2C correlated with CD8+ T-cell numbers in humanized mouse models. KIF2C expression is also associated to tumor-immune cells infiltration. The protein could be involved in promoting EC malignancy. Best Uses For The KIF2C Symbol

KIF23

KIF2C can be used in many ways. In addition to being an excellent tool for analyzing gene expression, this marker can help researchers better understand the functions of this protein. KIF2C can be used in many ways. These are the five best. Each pathway involves KIF2C and has its own best use. This article provides an overview of how to use KIF2C in various applications.

KIF2C plays a crucial role in solid tumors. It is involved in tumor cell proliferation, migration, metastasis, and metastasis. TMA Abdel Fatah (and colleagues) found that elevated levels of this protein were associated with poor prognosis in one study. Gnjatic, et al. Gnjatic et.al. discovered that KIF2C overexpressed in many solid tumor types, including lung carcinoma. In addition, Gan et al. demonstrated that KIF2C is regulated by miR325-3p and may have a role in leukemia.

CCK8 assays

Cell Counting Kit-8, also known as CCK-8, is a tool that uses human hepatoma to measure the proliferation of cancer cells. The kit includes reagents for amplifying total RNA, 10 uls of CCK-8 and a wavelength of 450 nm. It is compatible for use with HeLa cell lines. To perform the assay, the cells were seeded in 96-well plates, 2x103 cells per well, and the KIF2C marker. The cells were cultured for four hours and subsequently counted using a microplate reader. The data were averaged with a standard deviation of less than 2%.

The CCK8 assays using the KIP2C marker by Boster Bio have demonstrated improved detection rates when compared to conventional methods, including cell lysis and cell culture. Numerous studies have successfully validated the CCK8 method. The KIF2C protein is expressed in many types of tumors, including endometrial cancer (EC), and ovarian cancer. The KIF2C protein expression level varies from cancer cell to cancer cell.

Treatment with siRNA for KIF2C silence

The results of our study suggest that miR-548 regulates KIF2C expression. KIF2C expression in UMUC-3 and T24 cells is inhibited with miR-548 by the miR-548 inhibitor. KIF2C expression is suppressed in UMUC-3 cells and T24 cells by miR-548 downregulation. However, KIF2C overexpression causes increased cell proliferation and migration. We hypothesize that downregulation of miR-548 may help target KIF2C for BC treatment.

To evaluate the therapeutic efficacy of siRNA to silence KIF2C, we used a mouse model with subcutaneous tumors that were 1 cm in diameter. The pGPU6/GFP/Kif2a RNAi virus was intra-tumorally injected to 4 groups. After treatment, the animals were weighed weekly. The study found that siRNA to silence KIF2C reduces tumor growth in vivo, and increases the effectiveness of 5-Fu. Ultimately, the treatment with siRNA to silence KIF2C will depend on low toxicity and high efficacy of the KIF2a RNAi vector.

Ambion Kif2a siRNA was used for this study. This plasmid is 19-bp long and has a stem-loop structure. It is processed and directed at down-regulation by Dicer. Polymerase III enhancers were created to increase siRNA's efficiency. These promoters lack the termination signal and polymerase A tail that are required for efficient siRNA expression. Additionally, the study used polymerase II driven shRNA expression vectors.

Treatment with shNC

The mechanism of KIF2C signaling is unclear but may involve the Wnt/b-catenin pathway. This pathway was blocked by treatment with shNC for KIF2C markers in several cancers including HCC. One study showed that shNC treatment for KIF2C marker had a significant effect on tumor volume and mass. This therapy also reduced KIF2C levels in HCC-cells.

In the same study we examined the effects on cell growth of shNC for KIF2C markers in vitro. CCK8 assays were used to determine the effects of shNC on cell viability, proliferation, and other factors. The control cells were given puromycin. Treatment with shNC to the KIF2C marker significantly decreased Ishikawa cell colonies.

TBC1D7, which is an mTOR inhibitor, inhibits KIF2C-overexpressing HCC cell's migratory or invasive capabilities. KIF2C regulation is controlled by mTORC1. It can be used to treat HCC. It has the potential to prevent the progression of HCC. It also inhibits the growth of other tumor types, including lung cancer.