TTLL7: A Potential Drug Target and Biomarker (G79739)

Target Name: TTLL7

NCBI ID: G79739

TTLL7

TTLL7: A Potential Drug Target and Biomarker

TTLL7, short for T-cell long non-coding RNA, has been identified as a potential drug target and biomarker in various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. This gene has been shown to play a crucial role in the regulation of T-cell development and function, making it an attractive target for therapeutic intervention.

TTLL7 is a non-coding RNA that is expressed in various tissues and cells, including the brain, spinal cord, and peripheral tissues. It is composed of 19 exons, encoding a protein with a molecular weight of approximately 30 kDa. The protein produced by TTLL7 functions as a negative regulator of the NF-kappa-B signaling pathway, which is a well-established regulator of inflammation and immune responses.

The NF-kappa-B signaling pathway is a complex network of genes that play a crucial role in the regulation of cellular processes, including inflammation, cell survival, and transcriptional regulation. The activity of this pathway is regulated by various proteins, including the NF-kappa-B transcription factor, which is a key mediator of the pathway.

TTLL7 has been shown to play a negative role in the regulation of NF-kappa-B signaling pathway. It encodes a protein that can bind to the NF-kappa-B transcription factor and prevent its activity from driving the transcription of target genes. This interaction between TTLL7 and NF-kappa-B is critical for the regulation of T-cell development and function, as T-cells are known to play a major role in the immune response.

In neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, T-cell dysfunction is a hallmark feature. These diseases are characterized by the progressive loss of T-cells, which leads to an imbalance in the immune system and a increased risk of infections and other complications.

TTLL7 has been shown to be involved in the regulation of T-cell function in neurodegenerative diseases. For example, studies have shown that TTLL7 is downregulated in the brains of individuals with Alzheimer's disease, and that this downregulation is associated with an increased risk of cognitive impairment and other neurodegenerative symptoms.

In addition to its role in neurodegenerative diseases, TTLL7 has also been shown to be involved in the regulation of cancer development. For example, studies have shown that TTLL7 is downregulated in various types of cancer, and that this downregulation is associated with an increased risk of cancer progression and the development of invasive tumors.

TTLL7 has also been shown to be involved in the regulation of autoimmune disorders, such as rheumatoid arthritis and multiple sclerosis. These disorders are characterized by the production of antibodies that can cause inflammation and damage to body tissues.

In rheumatoid arthritis, for example, studies have shown that TTLL7 is downregulated in the peripheral tissues of individuals with rheumatoid arthritis, and that this downregulation is associated with an increased risk of the development of joint inflammation and damage.

In conclusion, TTLL7 is a gene that has been shown to play a crucial role in the regulation of T-cell development and function, as well as the regulation of neurodegenerative diseases, cancer, and autoimmune disorders. As such, TTLL7 is an attractive target for therapeutic intervention, and further research is needed to fully understand its role in these complex conditions.

Protein Name: Tubulin Tyrosine Ligase Like 7

Functions: Polyglutamylase which modifies tubulin, generating polyglutamate side chains of variable lengths on the gamma-carboxyl group of specific glutamate residues within the C-terminal tail of tubulin (PubMed:16901895, PubMed:25959773). Mediates both ATP-dependent initiation and elongation steps of the polyglutamylation reaction (PubMed:16901895, PubMed:25959773). Preferentially modifies the beta-tubulin tail over an alpha-tail (PubMed:16901895, PubMed:25959773). Competes with monoglycylase TTLL3 for modification site on beta-tubulin substrate, thereby creating an anticorrelation between glycylation and glutamylation reactions (By similarity). Required for neurite growth; responsible for the strong increase in tubulin polyglutamylation during postnatal neuronal maturation (By similarity)

The "TTLL7 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about TTLL7 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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