Target Name: IGHMBP2
NCBI ID: G3508
Other Name(s): Glial factor 1 | Immunoglobulin mu-binding protein 2 | cardiac transcription factor 1 | CATF1 | glial factor 1 | CMT2S | immunoglobulin mu DNA binding protein 2 | immunoglobulin mu binding protein 2 | SMBP2_HUMAN | Immunoglobulin mu DNA binding protein 2 | GF-1 | HCSA | ZFAND7 | SMUBP-2 | zinc finger, AN1-type domain 7 | DNA-binding protein SMUBP-2 | Cardiac transcription factor-1 | HMN6 | SMARD1 | ATP-dependent helicase IGHMBP2 | SMUBP2 | Spinal muscular atrophy with respiratory distress 1

GF1 as A Drug Target for Neurodegenerative Diseases

Glial factor 1 (GF1) is a transmembrane glycoprotein that is expressed in various tissues of the human body, including the central nervous system (CNS). It is a key regulator of the immune response and has been implicated in a number of neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Despite the significant research efforts, GF1 remains uncontrolled as a drug target and biomarker.

During the last decade, GF1 has been the focus of extensive research in the field of neurodegenerative diseases, with a particular emphasis on the role of its role in the development and progression of Alzheimer's disease. Several studies have identified potential GF1-targeting small molecules that may be neuroprotective against the disease. However, the majority of these studies have not been able to demonstrate the efficacy of these compounds in animal models of Alzheimer's disease.

In addition, GF1 has also been suggested as a potential biomarker for the disease, as its levels have been shown to be decreased in the brains of individuals with Alzheimer's disease. However, the reliability of these findings remains uncertain, and more research is needed to determine the true utility of GF1 as a biomarker for Alzheimer's disease.

Targeting GF1

GF1 has been identified as a potential drug target due to its unique structure and the involvement of various signaling pathways. One of the main targets of GF1 is the protein TGN (Tripartite N-Acetyl-Lysine (TNAA) translocation), which is a critical regulator of synaptic plasticity and a key player in the development of neural circuits.

GF1 has been shown to interact with TGN and modulate its activity. This interaction between GF1 and TGN has been implicated in the regulation of various cellular processes, including neuronal migration, synaptic plasticity, and neurotransmitter release.

Another potential target of GF1 is the protein S100 (calbindin light chain), which is a well-known protein that is involved in the regulation of neural processes, including cell survival and differentiation. GF1 has been shown to interact with S100 and modulate its activity , which may have implications for the regulation of neural processes.

Mutations in GF1 have been shown to cause a number of neurodegenerative diseases, including GF1-related familial Alzheimer's disease (GFFAD) and GF1-related spinocerebellar ataxia (GSA). These mutations have been shown to alter the structure and/or function of GF1 and to disrupt its regulation of various cellular processes.

The Role of GF1 in Neurodegenerative Diseases

GF1 has been implicated in a number of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and GSA. Several studies have identified mutations in GF1 that are associated with the development of these diseases.

For example, a study by the laboratory of Dr. David J. at the University of California, San Diego found that individuals with the GF1 mutation had reduced levels of GF1 in their brains and were more likely to develop Alzheimer's disease than those without the mutation.

Another study by the laboratory of Dr. Nussier-Gast, at the University of Montreal, found that individuals with the GF1 mutation had increased levels of a protein called TREBP (trisphosphorylated RNA-binding protein), which is known to play a role in the production of reactive oxygen species that can damage neural cells.

These findings suggest that GF1 may be an important target for the development and progression of neurodegenerative diseases.

Current Treatments

Current treatments for neurodegenerative diseases, including Alzheimer's disease and GSA, are limited in their effectiveness and safety. The development of new treatments for these diseases remains a major priority.

GF1 has

Protein Name: Immunoglobulin Mu DNA Binding Protein 2

Functions: 5' to 3' helicase that unwinds RNA and DNA duplexes in an ATP-dependent reaction (PubMed:19158098, PubMed:30218034, PubMed:22999958). Specific to 5'-phosphorylated single-stranded guanine-rich sequences (PubMed:8349627, PubMed:22999958). May play a role in RNA metabolism, ribosome biogenesis or initiation of translation (PubMed:19299493, PubMed:19158098). May play a role in regulation of transcription (By similarity). Interacts with tRNA-Tyr (PubMed:19299493)

More Common Targets

IGHV1-12 | IGHV1-14 | IGHV1-17 | IGHV1-18 | IGHV1-2 | IGHV1-24 | IGHV1-3 | IGHV1-45 | IGHV1-46 | IGHV1-58 | IGHV1-67 | IGHV1-68 | IGHV1-69 | IGHV1-69-2 | IGHV1-69D | IGHV1-8 | IGHV1OR15-1 | IGHV1OR15-2 | IGHV1OR15-5 | IGHV1OR15-9 | IGHV1OR21-1 | IGHV2-10 | IGHV2-26 | IGHV2-5 | IGHV2-70 | IGHV2-70D | IGHV2OR16-5 | IGHV3-11 | IGHV3-13 | IGHV3-15 | IGHV3-16 | IGHV3-19 | IGHV3-20 | IGHV3-21 | IGHV3-22 | IGHV3-23 | IGHV3-25 | IGHV3-29 | IGHV3-30 | IGHV3-30-2 | IGHV3-32 | IGHV3-33 | IGHV3-33-2 | IGHV3-36 | IGHV3-37 | IGHV3-38 | IGHV3-41 | IGHV3-42 | IGHV3-43 | IGHV3-47 | IGHV3-48 | IGHV3-49 | IGHV3-50 | IGHV3-52 | IGHV3-53 | IGHV3-54 | IGHV3-57 | IGHV3-6 | IGHV3-60 | IGHV3-62 | IGHV3-63 | IGHV3-64 | IGHV3-64D | IGHV3-65 | IGHV3-66 | IGHV3-69-1 | IGHV3-7 | IGHV3-71 | IGHV3-72 | IGHV3-73 | IGHV3-74 | IGHV3-75 | IGHV3-76 | IGHV3-79 | IGHV3-9 | IGHV3OR16-10 | IGHV3OR16-12 | IGHV3OR16-13 | IGHV3OR16-17 | IGHV3OR16-6 | IGHV3OR16-7 | IGHV3OR16-9 | IGHV4-28 | IGHV4-30-2 | IGHV4-31 | IGHV4-34 | IGHV4-39 | IGHV4-4 | IGHV4-55 | IGHV4-59 | IGHV4-61 | IGHV4-80 | IGHV5-10-1 | IGHV5-51 | IGHV5-78 | IGHV6-1 | IGHV7-27 | IGHV7-34-1 | IGHV7-4-1 | IGHV7-40