Stathmin-2 Antibodies

Stathmin-2 (STMN2)

Regulator of microtubule stability. When phosphorylated by MAPK8, stabilizes microtubules and consequently controls neurite length in cortical neurons.

In the developing brain, negatively regulates the rate of exit from multipolar phase and retards radial migration from the ventricular zone (By similarity). .

Gene Information

Human
Gene Name:	STMN2
Uniprot:	Q93045
Entrez:	11075

Family

Belongs to:
stathmin family

Alternative Names

FLJ34868; FLJ50995; neuron-specific growth-associated protein; Protein SCG10; SCG10; SCG10neuronal growth-associated protein (silencer element); SCGN10; SCGN10stathmin-2; Stathmin2; Stathmin-2; stathmin-like 2; STMN2; superior cervical ganglia, neural specific 10; Superior cervical ganglion-10 protein

Molecular Weight

Mass (kDA):
20.828 kDA

Genomic Context

Human
Location:	8q21.13
Sequence:	8; NC_000008.11 (79611117..79666162)

Tissue Specificity

Neuron specific.

Subcellular Localizations

Cytoplasm. Cytoplasm, perinuclear region. Cell projection, growth cone. Membrane; Peripheral membrane protein; Cytoplasmic side. Cell projection, axon. Golgi apparatus. Endosome. Cell projection, lamellipodium. Associated with punctate structures in the perinuclear cytoplasm, axons, and growth cones of developing neurons. SCG10 exists in both soluble and membrane-bound forms. Colocalized with CIB1 in neurites of developing hippocampal primary neurons (By similarity). Colocalized with CIB1 in the cell body, neuritis and growth cones of neurons. Colocalized with CIB1 to the leading edge of lamel

Diseases

• Nervousness
• Malignant Neoplasms
• Prion Diseases
• Pheochromocytoma
• New Variant Creutzfeldt-jakob Disease
• Liver Carcinoma
• Creutzfeldt-jakob Disease
• Crest Syndrome
• Sensory Denervation Disorder
• Alzheimer's Disease
• Hepatitis C, Chronic
• Fibrosis
• Neoplasms

• Hepatitis
• Hepatitis C
• Encephalopathy, Bovine Spongiform
• Hepatitis, Chronic
• Neuroblastoma
• Encephalopathies
• Down Syndrome

Interacting Proteins

• TEX11
• TFCP2
• TXLNA

Pathways

• Localization
• Regeneration
• Brain Development
• Transport
• Aging
• Cell Proliferation
• Golgi Localization
• Neurogenesis
• Interphase
• Microtubule Polymerization
• Mitosis
• Cell Migration
• Gene Silencing

• Protein Targeting
• Microtubule Depolymerization
• Axon Guidance
• Cell Differentiation
• Methylation
• Cell Death
• Cell Growth

PTMs

• Phosphorylation
• Palmitoylation

• Methylation
• Deacetylation

• Acetylation

Research Areas

• Neuroscience

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/STMN2

Boster Bio - The Best Uses Of The STMN2 Marker

This article will cover the advantages of using the STMN2 marker in research and development. It will cover its function, applications, history, and benefits. It is applicable to scientists worldwide. This article will also introduce you to the Boster Bio system. Read on to discover more. It's not only beneficial for research and development, but also for the use of scientists around the world.

Benefits of using the STMN2 Marker

STMN2 is a gene that has a number of functions and is highly expressed in the central nervous system. The gene's association with motor neuron degeneration has been studied by Harvard researchers. Specifically, they focused on STMN2 and how it interacts with TDP-43. In their study, the researchers found that lowering TDP-43 levels in cell nuclei resulted in the destruction of STMN2 instructions, which are necessary for the repair and growth of motor neuron axons.

Function

STMN2 is a member of the stathmin family, which binds tubulin and regulates microtubule dynamics. This protein is a membrane-associated neuronal protein with a high expression level correlated with neurite outgrowth. Its N-terminal domain regulates localization of the protein to the Golgi complex, where it targets growth cones. STMN2 also exists in membrane-bound and soluble forms.

Recent studies have found reduced STMN2 expression in Parkinson's disease and frontotemporal dementia. However, levels of full-length STMN2 were not always correlated with the burden of phosphorylated TDP-43 in patients with frontotemporal dementia. This suggests that other factors regulate STMN2 expression. The study's authors believe that functional alterations in these genes are responsible for the reduced STMN2 expression.

In a study, researchers examined the STMN2 CA genotype in 67 patients with sALS. The SALSA project recruited patients with a range of sALS-related disease, and they followed them over a period of up to 25 months. The study included information on patient demographics, as well as clinical information. In addition, genotypes were recorded to compare differences in STMN2 expression.

Functional analysis of the STMN2 gene showed that the presence of the 24 CA repeat was associated with a reduced basal level of expression. The results of this study also revealed that the TDP-43 mediated cryptic exon mechanism played a significant role in maintaining axonal outgrowth. In fALS, reduced STMN2 expression was observed in spinal motor neurons and motor cortex. This is likely associated with the C9orf72 repeat expansion, the most common cause of ALS.

In a separate study, researchers identified alleles with ten to twenty-six CA repeats. These alleles were confirmed by capillary fragment separation, and the seven-thousand base pairs were then mapped to a pre-mRNA structure. Interestingly, these alleles had the same pre-mRNA structure in both the control and the case groups. For a longer study, the RNA fold analysis of STMN2 revealed that a subset of these alleles contained an open-circular structure.

Applications

The STMN2 gene code for a member of the stathmin family of phosphoproteins. This protein has diverse functions including signal transduction and microtubule dynamics. It is thought to be involved in neuronal growth and development, as well as osteogenesis. It has been associated with Down's syndrome and Alzheimer's disease, and reduced expression of stathmin genes is associated with these conditions.

This discovery reveals an important role for SSV in regulating STMN2 gene expression and influencing the neurodegenerative disease phenotype. Further, the discovery of SSV and its application in the field of ALS adds to the growing body of evidence supporting the role of this gene in the disease. The development of the STMN2 genetic marker has implications in clinical assessment and therapeutic development. It can also serve as a useful tool for stratifying patient response in clinical trials.

History

Recent reports have indicated reduced STMN2 expression in patients with frontotemporal dementia and Parkinson's disease. These studies suggest that levels of full-length STMN2 are not always associated with phosphorylated TDP-43 burden. Thus, the authors suggest that other factors may regulate STMN2 expression. In this context, their study could help distinguish between TDP-43-positive and -negative cases.

Previous studies have demonstrated that the STMN2 CA repeat may be associated with ALS disease risk and disease-modifying effects. These findings confirmed that the presence of a 24 CA repeat is associated with disease risk and confirms the hypothesis that allele length is a determinant of risk, and short alleles are protective. However, the risk genotype group L/L (24 CA) was associated with decreased survival when adjusting for age at onset.

STMN2 is a member of the stathmin family of proteins that bind to tubulin and promote microtubule disassembly. It is an associated membrane-associated neuronal protein whose expression correlates with neurite outgrowth. Its unique N-terminal domain contributes to its localization in the Golgi complex, where it targets growth cones. STMN2 also exists in soluble and membrane-bound forms.

The truncated STMN2 gene was identified in mouse models of Parkinson's disease, a disease that affects axons. The researchers then demonstrated that reducing TDP-43 levels in motor neurons affected by TARDBP mutations resulted in reduced STMN2 expression. In addition, they found that STMN2 is required for normal axonal outgrowth and regeneration.

Because Stathmin-2 is an axonal growth and repair gene, STMN2 has been identified as a gene with therapeutic potential in ALS. It is linked to the ALS gene TARDBP, which is depleted or mislocalized in patients with ALS. In addition, a lack of effective treatment options for the disease has hampered efforts toward a cure. With this breakthrough, it may be possible to find a new drug that halts the disease's progression and improves quality of life for patients with ALS.

Researchers at the Perron Institute for Neurological and Translational Science, the Ian Potter Foundation, and the Racing for MNDi Foundation funded the research. These organizations have also funded the generation of olfactory neurosphere-derived cells. The RNA was then sequenced for STMN2 expression. Furthermore, a number of sALS cases were identified as containing increased levels of STMN2 mRNA.