Plasma kallikrein Antibodies

Plasma kallikrein (KLKB1)

The enzyme cleaves Lys-Arg and Arg-Ser bonds. It activates, in a mutual response, factor XII following its binding to a negatively charged surface.

Additionally, it releases bradykinin from HMW kininogen and may also play a role in the renin-angiotensin system by converting prorenin into renin. .

Gene Information

Human
Gene Name:	KLKB1
Uniprot:	P03952
Entrez:	3818

Family

Belongs to:
peptidase S1 family

Alternative Names

EC 3.4.21; EC 3.4.21.34; Fletcher factor; kallikrein B, plasma (Fletcher factor) 1; kininogenin; KLK3plasma kallikrein; KLKB1; plasma kallikrein heavy chain; plasma kallikrein light chain; Plasma Kallikrein; Plasma Prekallikrein; PPK

Molecular Weight

Mass (kDA):
71.37 kDA

Genomic Context

Human
Location:	4q35.2
Sequence:	4; NC_000004.12 (186215714..186258477)

Subcellular Localizations

Secreted.

Diseases

• Malignant Neoplasms
• Malignant Neoplasm Of Lung
• Venous Thrombosis
• Deep Vein Thrombosis
• Thrombosis
• Carcinoma
• Lung Neoplasms
• Thrombophilia
• Hypertensive Disease
• Essential Hypertension
• Stenosis
• Infarction
• Malignant Neoplasm Of Breast

• Pulmonary Embolism
• Thromboembolism
• Muscular Dystrophy, Facioscapulohumeral
• Unbalanced Translocation
• Carcinogenesis
• Myocardial Infarction
• Venous Thromboembolism

Pathways

• Coagulation
• Blood Coagulation
• Methylation
• Mammary Gland Involution
• Cell Proliferation
• Aging
• Dna Methylation
• Glycosylation

• Pathogenesis
• Localization
• Epithelial Cell Proliferation

PTMs

• Demethylation

• Biotinylation

• Methylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/KLKB1

Best Uses Of The KLKB1 Marker

The KLKB1 protein is a candidate to detect melanoma (a common form of Leukemia). Researchers are interested to quantify this novel transcript due to its potential clinical utility. Researchers trust Boster's primary antibody. They are highly specific and have high-affinity binding. For more information, visit bosterbio.com.

KLKs are implicated in human malignancies

The family of proteins encoded by the KLK genes includes a diverse set of serine proteases involved in several cellular processes. Human malignancies are caused by the deregulation and inhibition of KLK production and secretion. KLK activation in cancer cells may be a biomarker and therapeutic target. There are still many open questions regarding KLKs' role in human malignancies.

Different studies have examined KLK6's role in cancer. These studies revealed that KLK6 induces Ecadherin shedding which promotes cell migration, invasion and proliferation. KLK6 expression is controlled by Caveolin-1, which is a structural protein in caveolae. The overexpression of KLK6 in human tumors is associated with an increased cell growth rate, hyperproliferation, and accelerated cell cycles between the G1 and S phases.

Currently, there is no approved therapy that targets KLKs. Recent advances in the field have shown unexpected roles for KLKs. To better understand the function and role of these proteins for human malignancies, further research is needed. There are several promising KLK inhibitions on the marketplace. They should be able to target KLK6 without compromising their pharmacological activity.

KLK14, a key player in the development many types of cancer, is also implicated. KLK13 expression in cancer cells is not statistically significant when compared to KLK7 levels in normal tissues. However, it is associated with poor survival rates and disease-free survival among patients with cancer. KLK14 may play a role in the cancer response. The authors conclude that KLK14 involvement may contribute to the development of a tumor's inflammatory response, and that it is a strong prognostic factor for cancer.

Nuclear receptor signaling regulates KLK gene expression. KLK zymogen activation may be mediated by complex proteolytic cascades. KLK enzymes regulate many biological processes, including neurodegeneration, ECM degradation and remodeling, as well as neurodegeneration. KLKs have been shown to be novel tumor markers, as some KLKs are found in cancer cells. For this reason, research is required to better understand the function of these proteins in cancers.

Moreover, studies have revealed that some of the novel KLK family members may serve as a new independent marker of lung cancer. KLKs may also be associated with other types cancers, suggesting that these proteins may act as tumor specific biomarkers. However, further research is required to determine if KLK8-8-T4 can be used as a therapeutic target. The KLK8/T4 alternative splice variation is the most frequent mRNA isoform in lung tumor tissue.

KLK5 was discovered to be produced in the stratum grauulosum, the lowest layer of skin. The pH in this layer, which is almost neutral is higher than the stratum corneum, which is acidic and has a "sealed core". KLK5 activates in the stratumgranulosum and quashes its activity by binding with LEKTI fragments. KLK5/ mice show an increase in antimicrobial activity and a hypersensitive skin.

Clinical applications may be possible through the quantification of novel transcripts

Recent studies have shown RNA that contains novel gene expression is more stable and stable than those that are already known. This may have clinical implications. However, RNA destruction is a problem. Because RNA is rapidly destroyed, it is difficult to compare transcription levels between genes. The level of transcription may differ depending on the strand used to sequence the DNA. This can lead to mismeasured or missing DNA in the population.

RNA sequencing technology is a powerful diagnostic, prognostic, and therapeutic tool, allowing the detection of gene fusions and the differential expression of known disease-causing transcripts. Multifaceted clinical applications can also be made possible by the diverse RNA species found within human tissues. These novel RNAs can also be used to non-invasively diagnose various diseases. It is still necessary to improve the reproducibility for gene expression studies.

Because mRNA samples can be obtained from multiple tissues, the quality of mRNA templates may vary. This could be due to factors such as adapters and altered splicing events. Inconsistencies and poor sample handling can make it difficult to determine the quality of mRNA-templates. A variety of contaminating nucleases, genome DNA, and reverse transcriptase inhibitors may be found in clinical samples.

RTqPCR may also be useful for predicting a patient's response to targeted therapies. Patients with BCR–ABL1-positive chronic meeloid leukemia (CML) are well-served by kinase inhibitions. As such, qRTPCR with BCR-ABL1 transcripts is recommended as a clinical biomarker. Long-read RNA-seq may further enhance the utility of fusion transcript measurements by allowing for the detection of mutation phasing across the entire fusion transcript.

RNA-seq can be used to identify new genes and the associated gene expression. High-throughput DNA sequencing provides single-molecule information and whole-transcript data. Scientists can use this technology to reconstruct the transcriptome by sequencing unmapped sequences. It is difficult to reconstruct a sequence of novel transcripts with deep RNA sequencing data because of sequencing errors or alternative splicing. In addition, variants and modifications can complicate the alignment process. De-novo assembly presents a computational challenge.

This approach can be used in cancer research. For example, RNA-seq can help identify over-expressed gene expression. In a recent case, JAK1 expression was found to be significantly elevated in a child with lung metastasis. Ruxilitinib (a JAK1 inhibitor) significantly decreased the size of the tumors and helped to reduce the patient's body weight.

Despite these limitations and many promising targets for clinical use, the study still identified many promising targets. The study showed that expression levels of 61 RNAs displayed cyclical variation across tissues. It also found 42 transcripts with histone marks in the genomic loci of at most one type of cancer cell line. When it came to tumors, the majority of genes involved in their development were differentially expressed. Several of them were also linked to the expressions of neighboring genes.

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