SCG10/Stathmin-2 Antibody [D11B18]

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution

Application
IP, IHC

Reactivity
Human, Mouse, Rat

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
˜20 kDa

Positive Control	Adult rat neocortex; Adult rat hippocampus; Cultured hippocampal neurons (9 DIV)
Negative Control

Datasheet & SDS

Biological Description

Specificity
SCG10/Stathmin-2 Antibody [D11B18] detects endogenous levels of total SCG10/Stathmin-2 protein.

Clone
D11B18

Synonym(s)
Stathmin-2; Superior cervical ganglion-10 protein (Protein SCG10); Stmn2; Scg10; Scgn10

Background
SCG10 (Stathmin-2, STMN2) is a neuronally enriched microtubule destabilizing protein belonging to the stathmin family, essential for axonal outgrowth and regeneration. It contains an N-terminal regulatory domain with four key phosphorylation sites (Ser22, Ser25, Ser38, Ser63) that are targeted by kinases such as JNK1, MAPK, and PKA. The C-terminal region features an α-helical stathmin-like domain housing two tubulin-binding pockets, enabling SCG10 to sequester α/β-tubulin heterodimers in a 1:2 stoichiometry. This sequestration prevents longitudinal protofilament assembly and thus inhibits microtubule polymerization. In its dephosphorylated state, SCG10 binds free tubulin with high affinity (Kd ~0.3–1 μM), promoting microtubule catastrophe by shifting dynamics toward depolymerization through trapping GTPase-competent tubulin. Phosphorylation of SCG10, however, introduces negative charges and induces conformational changes that disrupt tubulin binding, thereby releasing tubulin heterodimers for microtubule growth. This mechanism stabilizes axonal microtubules during outgrowth. JNK1-mediated phosphorylation of Ser22/Thr22 is particularly important during cortical neuron migration, governing the transition from multipolar to bipolar morphology and modulating the speed of radial migration. SCG10 expression is highest in developing CNS neurons, where it mediates Ca²⁺-dependent microtubule remodeling via calmyrin binding, facilitating growth cone dynamics and contributing to axon regeneration following injury. Loss of TDP-43 in ALS/FTD leads to cryptic exon inclusion in STMN2 transcripts, resulting in depletion of functional SCG10 protein. This causes axonal degeneration, neuromuscular junction retraction, and motor deficits, phenotypes that can be reversed by restoring full-length STMN2 expression.

Background

SCG10 (Stathmin-2, STMN2) is a neuronally enriched microtubule destabilizing protein belonging to the stathmin family, essential for axonal outgrowth and regeneration. It contains an N-terminal regulatory domain with four key phosphorylation sites (Ser22, Ser25, Ser38, Ser63) that are targeted by kinases such as JNK1, MAPK, and PKA. The C-terminal region features an α-helical stathmin-like domain housing two tubulin-binding pockets, enabling SCG10 to sequester α/β-tubulin heterodimers in a 1:2 stoichiometry. This sequestration prevents longitudinal protofilament assembly and thus inhibits microtubule polymerization. In its dephosphorylated state, SCG10 binds free tubulin with high affinity (Kd ~0.3–1 μM), promoting microtubule catastrophe by shifting dynamics toward depolymerization through trapping GTPase-competent tubulin. Phosphorylation of SCG10, however, introduces negative charges and induces conformational changes that disrupt tubulin binding, thereby releasing tubulin heterodimers for microtubule growth. This mechanism stabilizes axonal microtubules during outgrowth. JNK1-mediated phosphorylation of Ser22/Thr22 is particularly important during cortical neuron migration, governing the transition from multipolar to bipolar morphology and modulating the speed of radial migration. SCG10 expression is highest in developing CNS neurons, where it mediates Ca²⁺-dependent microtubule remodeling via calmyrin binding, facilitating growth cone dynamics and contributing to axon regeneration following injury. Loss of TDP-43 in ALS/FTD leads to cryptic exon inclusion in STMN2 transcripts, resulting in depletion of functional SCG10 protein. This causes axonal degeneration, neuromuscular junction retraction, and motor deficits, phenotypes that can be reversed by restoring full-length STMN2 expression.

References
https://pubmed.ncbi.nlm.nih.gov/37236359/ https://pubmed.ncbi.nlm.nih.gov/39253877/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%