Target Name: FLCN
NCBI ID: G201163
Review Report on FLCN Target / Biomarker Content of Review Report on FLCN Target / Biomarker
FLCN
Other Name(s): Birt-Hogg-Dube syndrome protein | birt-Hogg-Dube syndrome protein | BHD skin lesion fibrofolliculoma protein | FLCL | Folliculin (isoform 2) | Folliculin | FLCN variant 1 | Folliculin, transcript variant 1 | FLCN_HUMAN | folliculin | BHD | Folliculin, transcript variant 2 | DENND8B | Folliculin (isoform 1) | FLCN variant 2

FLCN: Key Regulator of Protein Foldage and Cellular Processes

FLCN (Birt-Hogg-Dube syndrome protein) is a protein that is expressed in the liver and has been shown to play a role in the development and progression of various diseases, including cancer. It is also known as heat shock protein (HSP70) 22.5kDa. FLCN is a key regulator of the unfolded state of proteins and has been shown to be involved in a variety of cellular processes, including cell survival, apoptosis, and inflammation.

FLCN is a protein that is expressed in the liver and has been shown to play a role in the development and progression of various diseases, including cancer. It is also known as heat shock protein (HSP70) 22.5kDa. FLCN is a key regulator of the unfolded state of proteins and has been shown to be involved in a variety of cellular processes, including cell survival, apoptosis, and inflammation.

One of the key functions of FLCN is its role in regulating the unfolded state of proteins. Proteins are in a variety of different conformations, and FLCN plays a key role in ensuring that these proteins remain in their unfolded state and are not misfolded into their misfolded forms. This is important for the protein to perform its function correctly and to maintain cellular homeostasis.

FLCN has also been shown to be involved in cell apoptosis. Apoptosis is a natural process that helps remove damaged or dysfunctional cells from the body. FLCN has been shown to be involved in the regulation of cell apoptosis by promoting the formation of apoptotic bodies and activating caspases. This helps to maintain cellular homeostasis and prevent the spread of disease.

FLCN has also been shown to be involved in inflammation. Inflammation is a response of the immune system to harmful substances in the body. FLCN has been shown to be involved in the regulation of inflammation by preventing the activation and recruitment of immune cells. This helps to prevent chronic inflammation that can lead to a variety of diseases, including cancer.

FLCN is also a potential drug target. By targeting FLCN, researchers can study its role in various diseases and develop new treatments. For example, by inhibiting FLCN, researchers can study its role in cancer progression and develop new treatments for this disease. Additionally, by studying the regulation of FLCN, researchers can gain insights into the underlying mechanisms of cellular processes and develop new treatments for other diseases.

In conclusion, FLCN is a protein that plays a key role in the development and progression of various diseases, including cancer. It is also known as heat shock protein (HSP70) 22.5kDa and is expressed in the liver. FLCN is involved in the regulation of the unfolded state of proteins, cell apoptosis, and inflammation. As a result, FLCN is a potential drug target and can be used to study and treat a variety of diseases.

Protein Name: Folliculin

Functions: Multi-functional protein, involved in both the cellular response to amino acid availability and in the regulation of glycolysis (PubMed:17028174, PubMed:18663353, PubMed:21209915, PubMed:24081491, PubMed:24095279, PubMed:31704029, PubMed:31672913, PubMed:34381247). GTPase-activating protein that plays a key role in the cellular response to amino acid availability through regulation of the mTORC1 signaling cascade controlling the MiT/TFE factors TFEB and TFE3 (PubMed:17028174, PubMed:18663353, PubMed:21209915, PubMed:24081491, PubMed:24095279, PubMed:31704029, PubMed:31672913). Regulates glycolysis by binding to lactate dehydrogenase LDHA, acting as an uncompetitive inhibitor (PubMed:34381247). Activates mTORC1 by acting as a GTPase-activating protein: specifically stimulates GTP hydrolysis by RRAGC/RagC or RRAGD/RagD, promoting the conversion to the GDP-bound state of RRAGC/RagC or RRAGD/RagD, and thereby activating the kinase activity of mTORC1 (PubMed:24095279, PubMed:31704029, PubMed:31672913). The GTPase-activating activity is inhibited during starvation and activated in presence of nutrients (PubMed:31672913). Acts as a key component for mTORC1-dependent control of the MiT/TFE factors TFEB and TFE3, while it is not involved in mTORC1-dependent phosphorylation of canonical RPS6KB1/S6K1 and EIF4EBP1/4E-BP1 (PubMed:21209915, PubMed:24081491, PubMed:31672913). In low-amino acid conditions, the lysosomal folliculin complex (LFC) is formed on the membrane of lysosomes, which inhibits the GTPase-activating activity of FLCN, inactivates mTORC1 and maximizes nuclear translocation of TFEB and TFE3 (PubMed:31672913). Upon amino acid restimulation, RRAGA/RagA (or RRAGB/RagB) nucleotide exchange promotes disassembly of the LFC complex and liberates the GTPase-activating activity of FLCN, leading to activation of mTORC1 and subsequent cytoplasmic retention of TFEB and TFE3 (PubMed:31672913). Indirectly acts as a positive regulator of Wnt signaling by promoting mTOR-dependent cytoplasmic retention of MiT/TFE factor TFE3 (PubMed:31272105). Required for the exit of hematopoietic stem cell from pluripotency by promoting mTOR-dependent cytoplasmic retention of TFE3, thereby increasing Wnt signaling (PubMed:30733432). Acts as an inhibitor of browning of adipose tissue by regulating mTOR-dependent cytoplasmic retention of TFE3 (By similarity). Involved in the control of embryonic stem cells differentiation; together with LAMTOR1 it is necessary to recruit and activate RRAGC/RagC and RRAGD/RagD at the lysosomes, and to induce exit of embryonic stem cells from pluripotency via non-canonical, mTOR-independent TFE3 inactivation (By similarity). In response to flow stress, regulates STK11/LKB1 accumulation and mTORC1 activation through primary cilia: may act by recruiting STK11/LKB1 to primary cilia for activation of AMPK resided at basal bodies, causing mTORC1 down-regulation (PubMed:27072130). Together with FNIP1 and/or FNIP2, regulates autophagy: following phosphorylation by ULK1, interacts with GABARAP and promotes autophagy (PubMed:25126726). Required for starvation-induced perinuclear clustering of lysosomes by promoting association of RILP with its effector RAB34 (PubMed:27113757)

The "FLCN 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 FLCN 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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