Reck as a Drug Target: Unlocking the Potential of this Protein for Neurodegenerative Disorders

Target Name: RECK

NCBI ID: G8434

RECK

Other Name(s): RECK protein | hRECK | suppression of tumorigenicity 15 (reversion-inducing-cysteine-rich protein with kazal motifs) | Reversion inducing cysteine rich protein with kazal motifs, transcript variant 2 | Suppressor of tumorigenicity 15 protein | reversion inducing cysteine rich protein with kazal motifs | suppression of tumorigenicity 5 (reversion-inducing-cysteine-rich protein with kazal motifs) | suppressor of tumorigenicity 15 protein | RECK_HUMAN | Reversion-inducing cysteine-rich protein with Kazal motifs | ST15 | Reversion-inducing cysteine-rich protein with Kazal motifs (isoform 1) | RECK variant 2 | Reversion inducing cysteine rich protein with kazal motifs, transcript variant 1 | Reversion-inducing cysteine-rich protein with Kazal motifs (isoform 2) | membrane-anchored glycoprotein (metastasis and invasion) | RECK variant 1

Reck as a Drug Target: Unlocking the Potential of this Protein for Neurodegenerative Disorders

Introduction

Neurodegenerative diseases, such as Alzheimer's, Parkinson's, and Huntington's diseases, are characterized by the progressive loss of brain cells and the underlying mechanisms that support their growth and function. These conditions currently affect an average of 7 in 100,000 individuals, severely affecting Patient quality of life and health status. Although there are currently no specific drugs to treat these diseases, research is ongoing to find new treatments and drug targets. In recent years, scientists have discovered a protein called RECK that has significant neuroprotective effects and plays an important role in multiple neurodegenerative diseases. This article will explore the role of the RECK protein in neurodegenerative diseases and explore its possibility as a potential drug target.

The role of RECK protein

RECK (Regulation and Education of Cells) protein plays an important role in cell differentiation, cell cycle, apoptosis, cell signaling, etc. In neurons, RECK protein is mainly involved in neuronal growth, development, synapse formation and neuronal apoptosis. Neuronal apoptosis is an important neuroprotective mechanism that plays a key role in the process of neuronal damage and death.

In neurodegenerative diseases, neuronal apoptosis is often deranged, leading to nerve cell death and loss of neurological function. The RECK protein plays a key role in regulating neuronal apoptosis. Studies have shown that knockdown of the RECK gene can lead to increased neuronal apoptosis and aggravated neuronal damage, thereby increasing the risk of neurodegenerative diseases. Overexpression of RECK protein inhibits neuronal apoptosis, thereby improving the risk of neuronal damage and neurodegenerative diseases.

In addition, RECK protein also plays an important role in neuronal synapse formation. Neuronal synapses are an important pathway for information transmission between neurons, and RECK protein is involved in the establishment and maintenance of neuronal synapses. Therefore, in neurodegenerative diseases, abnormal expression of RECK protein may also be related to neuronal synapses. Related to abnormal formation.

Biological functions of RECK protein

The role of RECK protein in neurodegenerative diseases is also reflected in other biological functions.

1. Neuroprotective effect: RECK protein has a significant neuroprotective effect and can slow down the damage and death of neurons. Studies have shown that the RECK protein can protect neurons by regulating neuronal apoptosis, thereby improving neurological function in patients with neurodegenerative diseases.

2. Neuronal self-renewal: RECK protein can promote the self-renewal of neurons, thereby maintaining the relative stability of neuronal cell numbers. This could help improve neurological function in patients with neurodegenerative diseases and extend their lives.

3. Remodeling of neuronal connections: RECK protein can participate in the remodeling of neuronal connections, thereby improving the information transmission function between neurons. This helps improve neurological function in patients with neurodegenerative diseases and improves patients' quality of life.

4. Neuron metabolism regulation: RECK protein can participate in the metabolism regulation of neurons, thereby regulating the growth and development of neurons. This helps improve neurological function in patients with neurodegenerative diseases and promotes the self-renewal of nerve cells.

Drug targets for RECK proteins

RECK protein has important biological functions in neurodegenerative diseases and therefore has high value as a drug target. Currently, a variety of drugs have been studied on the RECK protein, including inhibitors, antagonists, and agonists.

1. Inhibitors: Some studies have shown that inhibiting the activity of the RECK protein can improve neurological function in patients with neurodegenerative diseases. These medications include antidepressants, antipsychotics, antiepileptics, and more.

2. Antagonists: Some studies have shown that antagonizing the activity of RECK protein can slow down the apoptosis of neurons, thereby improving neurological function in patients with neurodegenerative diseases. These drugs include anti-epileptic drugs, antidepressants, etc.

3. Agonists: Some studies have shown that stimulating the activity of RECK protein can promote neuronal apoptosis, thereby improving neurological function in patients with neurodegenerative diseases. These medications include antipsychotics, among others.

4.

Protein Name: Reversion Inducing Cysteine Rich Protein With Kazal Motifs

Functions: Functions together with ADGRA2 to enable brain endothelial cells to selectively respond to Wnt7 signals (WNT7A or WNT7B) (PubMed:28289266, PubMed:30026314). Plays a key role in Wnt7-specific responses: required for central nervous system (CNS) angiogenesis and blood-brain barrier regulation (By similarity). Acts as a Wnt7-specific coactivator of canonical Wnt signaling by decoding Wnt ligands: acts by interacting specifically with the disordered linker region of Wnt7, thereby conferring ligand selectivity for Wnt7 (PubMed:30026314). ADGRA2 is then required to deliver RECK-bound Wnt7 to frizzled by assembling a higher-order RECK-ADGRA2-Fzd-LRP5-LRP6 complex (PubMed:30026314). Also acts as a serine protease inhibitor: negatively regulates matrix metalloproteinase-9 (MMP9) by suppressing MMP9 secretion and by direct inhibition of its enzymatic activity (PubMed:9789069, PubMed:18194466). Also inhibits metalloproteinase activity of MMP2 and MMP14 (MT1-MMP) (PubMed:9789069)

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•   the target screening and validation;
•   expression level;
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