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- Table of Contents
Facts about LIM domain kinase 2.
Human | |
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Gene Name: | LIMK2 |
Uniprot: | P53671 |
Entrez: | 3985 |
Belongs to: |
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protein kinase superfamily |
EC 2.7.11.1; LIM domain kinase 2; LIMK-2
Mass (kDA):
72.232 kDA
Human | |
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Location: | 22q12.2 |
Sequence: | 22; NC_000022.11 (31212298..31280080) |
Highest expression in the placenta; moderate level in liver, lung, kidney, and pancreas. LIMK2a is found to be more abundant then LIMK2b in liver, colon, stomach, and spleen, while in brain, kidney, and placenta LIMK2b is the dominant form. In adult lung, both LIMK2a and LIMK2b is nearly equally observed.
Cytoplasm. Nucleus. Cytoplasm, cytoskeleton, spindle.; [Isoform LIMK2a]: Cytoplasm. Nucleus. Isoform LIMK2a is distributed in the cytoplasm and the nucleus.; [Isoform LIMK2b]: Cytoplasm. Nucleus. Isoform LIMK2b occurs mainly in the cytoplasm and is scarcely translocated to the nucleus.
The LIMK2 marker is a common name for parents, students, professionals, and parents. How can it help you? This article will cover the positive and negative aspects of the marker as well as the alternative. Continue reading for more information! Remember that you are not the only one searching for information on this marker. Many people have searched the internet for information on this particular marker.
There are many potential uses for LIMK2 markers. One possible use is as a tumor marker. Researchers discovered that LIMK2 was downregulated by several cancer cell lines with high potential metastatic potential in a recent study. This suggests that LIMK2 may be involved in the progression or certain types of cancer. It may also help researchers to understand how LIMK2 regulates different types of cell proliferation.
To determine the expression level of LIMK2 in human cells, total RNA from tumor samples and cells was extracted using the RNA Universal Tissue Kit Qiagen. Using the primers designed for LIMK2, we carried out quantitative RT-PCR for gene expression measurements. We used GAPDH for an internal control gene and normalized the LIMK2 expression to GAPDH transcript level.
LIMKs are closely associated with the immune system. This marker is particularly useful in studying the formation of the cortical structures. These findings will assist researchers in deciding how to target LIMKs in the development of healthy and diseased individuals. LIMK2 is important for normal cortical development and can also help determine the severity or risk of various diseases, including cancer. The comprehensive report will include the results of the study.
In addition to its potential roles in tumorigenesis, LIMK2 has multiple functions in the development of BC. LIMK2 is expressed in BC tissues to promote proliferation. In contrast, LIMK2 depletion caused a decrease in invasion and growth arrest in UMUC-3 BC-cells. In a mouse model of cancer, UMUC-3BC cells that were overexpressing LIMK2 grew larger tumors than those that were LIMK2 deficient.
LIMK2 is negatively correlated with other immune markers including PDCD1 (a tumor marker) and CD274 (a three-factor factor that are essential for the immune response). LIMK2 expression was also negatively correlated to CTLA-4, which is a tumor marker. The results showed that LIMK2 expression decreased the proliferation and immune infiltration of UM-UC-3 cells, which suggests a potential for a prognostic marker in LUSC.
The LIMK2 gene in the human genome is a highly conserved transcript factor. The gene's 3'-UTR contains several motifs which can facilitate the spatial regulation of actin polymerization in spines. The LIMK2 genetic marker was made by cloning genomic DNA fragments to a psiCHECK-2 plasmid vector and using Gateway Technology to modify the gene. The resulting vector contained the LIMK2 gene reporter encompassing the first 251 and 126 bp of the 3'-UTR.
Palmitoylation, while it is not required to immobilize LIMK1, plays an important role for LIMK1's localization and activity. The authors should discuss LIMK1 palmitoylation and LIMK1 localization within neurons. They should also address the specific comments from their review and incorporate them in the manuscript. A discussion of upstream LIMK1 Palmitoylation should also be included.
LIMK2 (or LIMK2) is an essential protein that regulates cell growth. It is expressed in a variety cells in the body including the bladder. LIMK2 overexpression of cells can enhance the ability of cells to undergo the cell cycle. LIMK2 can be overexpressed in cells, which results in a faster rate for proliferation. They also have a higher ability to invade other cells and metastasize.
There is no conclusive correlation between LIMK2 levels and certain human diseases. The research on LIMK gene is still in its early stages. It is not yet clear if the gene is related with human diseases. It is worth recognizing that LIMK's gene activity is an indicator that other kinases are present and not LIMK. It could still be of value in other applications. It may be of some value in other applications.
LIMK1 as well as LIMK2 are also important in brain development. They regulate the stability and activity-dependent morphological plasticity of the dendritic spine actin. Further, LIMK1 is essential in the regulation of actin at the spine and subspine level. Its palmitoylation allows for the targeting of LIMK1 or PAK in neurons.
The LIMK1 receptor is the key regulator of BMP receptor activity. In neurons, this protein regulates morphology and activity-dependent morphological plasticity. Normal spine actin turnover is dependent on LIMK1. It also controls activation of PAK in neurons. Its palmitoylation makes it possible to regulate actin at the subspine as well as single-spine levels.
The LIMK1 as well as LIMK2 genes are closely related. Both genes regulate actin monomerization and their localization. LIMK1 & LIMK2 both play an important role in the regulation synaptic plasticity, spine development, and their localization. LIMK1 expression is enhanced in spines in mice. LIMK2 is also found in unfavorable tissues such as the colon, kidneys, and heart.
LIMK2 is also associated with epithelial-mesenchymal transition. LIMK2 expression was less in cell lines with high levels of metastatic potential. A decrease in LIMK2 expression could be a factor in the development of CRC. Further studies are needed to confirm whether LIMK2 plays a role in this process. LIMK2-silencing was linked to higher tumor nodules, faster progression and more metastasis in mice.
When LIMKs are used as an epigenetic marker, they may affect dendritic spines of auditory nerves. LIMKs are abundant in the brain and may be altered by epigenetic modification. The LIMK2 mutation was accidentally discovered. It is currently being studied to determine its role in epigenetic control of neurotransmitters.
LIMK2 is a target for cancer therapy. Studies suggest that it may be beneficial in chemotherapy. It is involved with dysfunction and function in the central nervous systems. A poor prognosis for AML is associated with the overexpression of this protein. Several factors may influence its expression, including genetic background. These issues will be discussed in this review, as well as other uses of LIMK2 proteins. However, some questions remain.
In addition to being involved in fetal development, LIMKs have been linked to a variety of neurological and mental disorders. These conditions could be due to LIMK dependence abnormalities in brain. LIMKs play a crucial role in normal cortical function and development. They are also involved with many types of breast cancer. Researchers are currently investigating the role of LIMK2 genes in cancer.
There is a growing body of research into alternative uses of the LIMK2 marker. LIMK2-silencing in liver tumor cells led to an increase in tumor nodules, metastasis and other markers. This suggests that LIMK2 could play a role in the progression of CRCs. Furthermore, it may also serve as a tumor marker. And although the LIMK2 gene is not directly involved in cancer development, it may help physicians understand how to improve treatment outcomes.
LIMK2 may be a prognosticant for patients with acute meeloid leukemia. It also regulates synaptic activities and promotes neuronal differentiate. In mice, LIMK1 regulates the L-LTP protein in neurons. Tob is a protein which is involved in cellular proliferation and is a substrate LIMK1.
LIMK1 and LIMK2 regulate cell cycle transition. LIMK2 regulates the cofilin phosphorylation that is essential for proper mitotic spinningle positioning. LIMK2 regulates the activity Aurora kinase. LIMK is essential for cell polarity, and neurogenesis. Read the article below to learn more about LIMK's role.
PMID: 8537403 by Okano I., et al. Identification and characterization of a novel family of serine/threonine kinases containing two N-terminal LIM motifs.
PMID: 8954941 by Osada H., et al. Subcellular localization and protein interaction of the human LIMK2 gene expressing alternative transcripts with tissue-specific regulation.