Fodrin, also referred to as non-erythroid (αII-; brain) spectrin, is a tetrameric (αγ)2 actin-binding, fibrous protein, widely distributed in vertebrates, which forms part of the sub-membranous cytoskeleton within many cell types including neurons, and is particularly abundant with axons. The α-subunits of fodrins and spectrin are highly conserved phylogenetically, with the exception of human α-fodrin, which shares only 55-59% homology with erythroid-specific α-spectrins. The β-subunits of spectrin (and γ-subunits of fodrins) are species specific. The interleukin-1 converting enzyme (ICE) family of proteases has been implicated as important effectors of the apoptotic pathway, perhaps acting hierarchically in a protease cascade. Neuronal fodrin is known to be cleaved by calpain following ischaemic insult and it has been proposed that calpain and an unidentified protease play a role in the onset of neuronal death following transient forebrain ischaemia. Recently, an ICE-like protease has been implicated in the early cleavage of fodrin, producing a 150kDa fragment, proximal to CPP32 in Fas-induced and C2-ceramide mediated apoptosis. A cleavage product of α-fodrin has been proposed as a candidate autoantigen in primary Sjögren’s syndrome and α-fodrin has been shown to be the source of a so-called ‘inhibitory protein factor’ family, members of which have been shown to inhibit both GABA and ATP-dependent glutamate uptake into purified synaptic vesicles.
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Rat primary septo-hippocampal co-cultures (astrocytes and neurons cultured from day E18 rat embyros) were challenged with the pro-apoptotic compound staurosporine or with vehicle (DMSO) for times indicated above. Protein (40 μg) was separated by SDS-PAGE, transferred to PVDF membrane and probed with FG6090. The caspase-3 cleaved 120-kDa fragment of alpha-II-spectrin was detected at a dilution of 1:4000. Western blot provided by courtesy of Dr Brian Pike, University of Florida.

Activation of caspase-3 and calpain in neonatal HI mice after AAT treatment. (A) The photomicrographs show immunochemistry staining of activated caspase-3 in the cortex (Cx), hippocampus (CA1), habenula nucleus (HN), and striatum (Str) at 24 h after HI in the vehicle-treated and AAT-treated groups. (B) Quantification of cleaved caspase-3-labeled cells at 24 h after HI in the Cx, CA1, HN, and Str (n = 14/group, p = 0.005 in Cx, p = 0.437 in CA1, p = 0.006 in HN, p = 0.001 in Str). (C) Quantification of cleaved caspase-3-labeled cells in the cortex at 24 h after HI in male and female mice (n = 7/group, p = 0.008 for males and p = 0.193 for females). (D) Quantification of cleaved caspase-3-labeled cells in the habenula nucleus at 24 h after HI in male and female mice (n = 7/group, p = 0.028 for males and p = 0.067 for females). (E) Quantification of cleaved caspase-3-labeled cells in the striatum at 24 h after HI in male and female mice (n = 7/group, p = 0.059 for males and p = 0.006 for females). (F) The caspase-3 activity in cortical tissue homogenate was measured at 24 h after HI in the AAT-treated and vehicle-treated groups (Veh = 12, AAT = 11, p = 0.011). (G) Measurement of caspase-3 activity at 24 h after HI in male and female mice (Veh = 6, AAT = 5, p = 0.273 in male; n = 6/group, p = 0.015 in female). (H) Representative immunoblotting of fodrin and actin in the cortical tissue from the injured hemisphere of the vehicle and AAT treatment groups at 24 h after HI. (I) Quantification of 120 kDa fragment expression at 24 h after HI in vehicle-treated and AAT-treated groups (n = 12/group, p = 0.024). (J) Quantification of 145/150 kDa fragment expression at 24 h after HI in vehicle-treated and AAT-treated groups (n = 12/group, p = 0.002). (K) Quantification of 120 kDa fragment expression at 24 h after HI in male and female mice (n = 6/group, p = 0.051 for males and p = 0.097 for females). (L) Quantification of 145/150 kDa fragment expression at 24 h after HI in male and female mice (n = 6/group, p = 0.007 for males and p = 0.086 for females). *p < 0.05, **p < 0.01.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Alpha1-antitrypsin protects the immature mouse brain following hypoxic-ischemic injury. Front Cell Neurosci (2023)

Selection of the best SNP targets.Primary Hu97/18 neurons were treated with 5e-9-5e ASOs targeted to 10 HD-SNPs at 6–1000 nM for 6 days. (A) HTT Western blots and quantitation for the 4 SNPs with the greatest activity. HTT levels are normalized to the internal loading control calnexin and then to the untreated sample for each allele. (B) Western blots showing full length and cleaved spectrin for the 4 ASOs. Spectrin fragment is normalized to calnexin and then to the untreated sample. Membranes were probed for HTT and reprobed for spectrin. Representative images are shown. n = 4–8 per data point. Data are presented as mean ± SD. Two way ANOVA with Bonferroni post hoc test have been performed and p values are illustrated with *, **, ***, **** for p = 0.05, 0.01, 0.001, and 0.0001. The PS backbone is black and MOE modifications are illustrated by orange. The SNP is underlined. The red dashed line represents the toxicity threshold.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Allele-specific suppression of mutant huntingtin using antisense oligonucleotides: providing a therapeutic option for all Huntington disease patients. PLoS One (2014)

SQSTM1 plays a role in early secondary brain damage formation after TBI. Lesion volume of SQSTM1−/− mice is reduced compared with SQSTM1+/+ littermates 24 h after experimental TBI (A). 5 days after trauma there is no difference between SQSTM1−/− and SQSTM1+/+ mice. Representative cresyl-violet stained sections at the coronal plane from 1.70 mm anterior to bregma, 0.46 mm posterior to bregma, and 1.46 mm posterior to bregma at 24 h (A) and 5 days (B) after CCI are shown (according to The Mouse Brain Library: www.mbl.org). Protein analysis was performed by immunoblotting to determine 120 and 145 kDa αII-spectrin fragments in perilesional brain tissue samples. In SQSTM1−/− mice calpain-dependent spectrin proteolysis to 145/150-kDa fragments is reduced by trend 24 h after CCI (C). There is no effect on calpain-dependent cell death 5 days after CCI (D). SQSTM1−/− does not influence caspase-dependent spectrin proteolysis to 120-kDa fragments (E,F). SQSTM1, sequestosome 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase, data are expressed as mean ± S.D. *P < 0.05.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice. Front Neurosci (2018)

SQSTM1 plays a role in early secondary brain damage formation after TBI. Lesion volume of SQSTM1−/− mice is reduced compared with SQSTM1+/+ littermates 24 h after experimental TBI (A). 5 days after trauma there is no difference between SQSTM1−/− and SQSTM1+/+ mice. Representative cresyl-violet stained sections at the coronal plane from 1.70 mm anterior to bregma, 0.46 mm posterior to bregma, and 1.46 mm posterior to bregma at 24 h (A) and 5 days (B) after CCI are shown (according to The Mouse Brain Library: www.mbl.org). Protein analysis was performed by immunoblotting to determine 120 and 145 kDa αII-spectrin fragments in perilesional brain tissue samples. In SQSTM1−/− mice calpain-dependent spectrin proteolysis to 145/150-kDa fragments is reduced by trend 24 h after CCI (C). There is no effect on calpain-dependent cell death 5 days after CCI (D). SQSTM1−/− does not influence caspase-dependent spectrin proteolysis to 120-kDa fragments (E,F). SQSTM1, sequestosome 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase, data are expressed as mean ± S.D. *P < 0.05.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice. Front Neurosci (2018)

SQSTM1 plays a role in early secondary brain damage formation after TBI. Lesion volume of SQSTM1−/− mice is reduced compared with SQSTM1+/+ littermates 24 h after experimental TBI (A). 5 days after trauma there is no difference between SQSTM1−/− and SQSTM1+/+ mice. Representative cresyl-violet stained sections at the coronal plane from 1.70 mm anterior to bregma, 0.46 mm posterior to bregma, and 1.46 mm posterior to bregma at 24 h (A) and 5 days (B) after CCI are shown (according to The Mouse Brain Library: www.mbl.org). Protein analysis was performed by immunoblotting to determine 120 and 145 kDa αII-spectrin fragments in perilesional brain tissue samples. In SQSTM1−/− mice calpain-dependent spectrin proteolysis to 145/150-kDa fragments is reduced by trend 24 h after CCI (C). There is no effect on calpain-dependent cell death 5 days after CCI (D). SQSTM1−/− does not influence caspase-dependent spectrin proteolysis to 120-kDa fragments (E,F). SQSTM1, sequestosome 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase, data are expressed as mean ± S.D. *P < 0.05.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice. Front Neurosci (2018)

Targeting two variants of a single HD-SNP to provide a therapeutic option to all HD patients.(A) The genotypes for the sequenced HD population at rs7685686. Green = heterozygous HD population (rs7685686_A/G, 48.7%, targetable by A-series ASOs and rs7685686_G/A, 3.8%, targetable by X-series ASOs). Blue = homozygous HD population (rs7685686_A/A, 44.9%, targetable by A-series ASOs and rs7685686_G/G, 2.6%, targetable by X-series ASOs). Primary YAC128 neurons were treated with ASO at 16–1000 nM for 6 days. (B) Western blot and quantitation of HTT protein levels. HTT levels are normalized to the internal loading control calnexin and then to the untreated sample for each allele. (C) Western blots showing full length and cleaved spectrin. Spectrin fragment is normalized to calnexin and then to the untreated sample. Membranes were probed for HTT and reprobed for spectrin. Representative images are shown. n = 8–12 per data point. Data are presented as mean ± SD. Two way ANOVA with Bonferroni post hoc test have been performed and p values are illustrated with *, **, ***, **** for p = 0.05, 0.01, 0.001, and 0.0001. The PS backbone is represented by black. MOE and cEt modifications are illustrated by orange and blue, respectively. The SNP is underlined. The red dashed line represents the toxicity threshold.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Allele-specific suppression of mutant huntingtin using antisense oligonucleotides: providing a therapeutic option for all Huntington disease patients. PLoS One (2014)

SQSTM1 plays a role in early secondary brain damage formation after TBI. Lesion volume of SQSTM1−/− mice is reduced compared with SQSTM1+/+ littermates 24 h after experimental TBI (A). 5 days after trauma there is no difference between SQSTM1−/− and SQSTM1+/+ mice. Representative cresyl-violet stained sections at the coronal plane from 1.70 mm anterior to bregma, 0.46 mm posterior to bregma, and 1.46 mm posterior to bregma at 24 h (A) and 5 days (B) after CCI are shown (according to The Mouse Brain Library: www.mbl.org). Protein analysis was performed by immunoblotting to determine 120 and 145 kDa αII-spectrin fragments in perilesional brain tissue samples. In SQSTM1−/− mice calpain-dependent spectrin proteolysis to 145/150-kDa fragments is reduced by trend 24 h after CCI (C). There is no effect on calpain-dependent cell death 5 days after CCI (D). SQSTM1−/− does not influence caspase-dependent spectrin proteolysis to 120-kDa fragments (E,F). SQSTM1, sequestosome 1; GAPDH, glyceraldehyde-3-phosphate dehydrogenase, data are expressed as mean ± S.D. *P < 0.05.
Image collected and cropped by CiteAb under a CC-BY license from the following publication: Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice. Front Neurosci (2018)








Product Details
Alternative Name |
αII-spectrin |
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Application |
IHC, WB |
Clone |
AA6 |
Formulation |
Liquid. In PBS containing 1.0% BSA and 0.09% sodium azide. |
Host |
Mouse |
Immunogen |
Chicken blood cell membranes following hypotonic lysis and mechanical enucleation. |
Isotype |
IgG1 |
Purity Detail |
Partially purified. |
Species Reactivity |
Chicken, Mammalian |
UniProt ID |
P07751 |
Worry-free Guarantee |
This antibody is covered by our Worry-Free Guarantee. |
Handling & Storage
Use/Stability |
Store unopened vial at -20°C until required for use. AVOID REPEATED FREEZE-THAW CYCLES. Aliquot undiluted antibody into smaller volumes (not less than 10μL) prior to freezing if appropriate. The use of high quality ‘antiserum-grade’ plastic or glass vials is recommended. Store diluted antibody at 2-4°C (do not freeze) and use within 1 month. Dilute to working strength with 50mM Tris-HCl buffer (pH 7.6) containing 1.5% sodium chloride and 1% normal goat serum (if a goat anti-mouse IgG linker antibody is to be used). |
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Long Term Storage |
-20°C |
Shipping |
Blue Ice |
Regulatory Status |
RUO – Research Use Only |
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- H3K14 lactylation exacerbates neuronal ferroptosis by inhibiting calcium efflux following intracerebral hemorrhagic stroke: Sun, T., Zhang, J. N., et al.; Cell Death Dis. 16, 553 (2025), Abstract
- Memantine Exacerbates Trimethyltin-Induced Neurodegeneration and Delays Cognitive Impairment Recovery: Onaka, Y., Yamaguchi, T., et al.; Neuropsychopharmacol. Rep. 45, e70014 (2025), Abstract
- Melatonin at repeated doses alleviates hyperglycemia-exacerbated cerebral ischemia-reperfusion injury at 72 h via anti-inflammation and anti-apoptosis.: Xu, Q., Cheung, R. T. F., et al.; IBRO Neurosci. Rep. 16, 418 (2024), Reactant(s): Rat, Abstract
- Efficacy of a cysteine protease inhibitor compared with enalapril in murine heart failure models: Aluja, D., Delgado-Tomás, S., et al.; iScience 27, 110935 (2024), Abstract
- Sortilin is dispensable for secondary injury processes following traumatic brain injury in mice.: Staib-Lasarzik, I., Gölz, C., et al.; Heliyon 10, e35198 (2024), Reactant(s): Mouse, Abstract
- Lifelong Chronic Sleep Disruption in a Mouse Model of Traumatic Brain Injury: Morris, A. R., Gudenschwager Basso, E. K., et al.; Neurotrauma Rep. 5, 61 (2024), Abstract
- A surge of cytosolic calcium dysregulates lysosomal function and impairs autophagy flux during cupric chloride-induced neuronal death.: Kim, Y., Lee, Y., et al.; J. Biol. Chem. 300, 105479 (2024), Reactant(s): Mouse, Abstract
- Neuronal RBM5 modulates cell signaling responses to traumatic and hypoxic-ischemic injury in a sex-dependent manner: Snyder, K., Gorse, K., et al.; Cell Death Discov. 9, 379 (2023), Abstract
- Melatonin mitigates type 1 diabetes-aggravated cerebral ischemia-reperfusion injury through anti-inflammatory and anti-apoptotic effects.: Xu, Q., Cheung, R. T. F., et al.; Brain Behav. 13, e3118 (2023), Application(s): WB / Reactant(s): Rat, Abstract
- Alpha1-antitrypsin protects the immature mouse brain following hypoxic-ischemic injury.: Zhang, S., Li, W., et al.; Front. Cell. Neurosci. 17, 1137497 (2023), Application(s): WB / Reactant(s): Mouse, Abstract
- Inhibition of autophagy in microglia and macrophages exacerbates innate immune responses and worsens brain injury outcomes.: Hegdekar, N., Sarkar, C., et al.; Autophagy 19, 2026 (2023), Reactant(s): Mouse, Abstract
- Sleep Disruption in a Mouse Model of Chronic Traumatic Brain Injury: Morris, A. R., Gudenschwager-Basso, E. K., et al.; bioRxiv , (2023), Application(s): WB
- Neurobiochemical, Peptidomic, and Bioinformatic Approaches to Characterize Tauopathy Peptidome Biomarker Candidates in Experimental Mouse Model of Traumatic Brain Injury: H. Yadikar, et al.; Mol. Neurobiol. 60, 2295 (2023), Abstract
- Influence of traumatic brain injury on ipsilateral and contralateral cortical perfusion in mice: S. Meyer, et al.; Neurosci. Lett. 795, 137047 (2023), Abstract
- Impairment of μ-calpain activation by rhTNFR:Fc reduces severe burn-induced membrane disruption in the heart: M.S. Cao, et al.; Cell Death Discov. 8, 10 (2022), Application(s): WB / Reactant(s) Rat, Abstract
- Characterization of Calpain and Caspase-6-Generated Glial Fibrillary Acidic Protein Breakdown Products Following Traumatic Brain Injury and Astroglial Cell Injury.: Yang, Z., Arja, R. D., et al.; Int. J. Mol. Sci. 23, (2022), Application(s): WB, Abstract
- Characterization of Calpain and Caspase-6 Generated Glial Fibrillary Acidic Protein Breakdown Products Following Traumatic Brain Injury and Astroglial Cell Injury: Yang, Z., Arja, R. D., et al.; Preprints.org , (2022), Application(s): WB
- The effect of clopidogrel and aspirin on the severity of traumatic brain injury in a rat model: F. Kobeissy, et al.; Neurochem. Int. 154, 105301 (2022), Abstract
- RNA Binding Motif 5 Gene Deletion Modulates Cell Signaling in a Sex-Dependent Manner but Not Hippocampal Cell Death: Farooq, J., Snyder, K., et al.; J. Neurotrauma 39, 577 (2022), Abstract
- Traumatic Brain Injury Induces cGAS Activation and Type I Interferon Signaling in Aged Mice.: Stoica, B. A., Loane, D. J., et al.; Front. Immunol. 12, 710608 (2021), Application(s): WB / Reactant(s): Mouse, Abstract
- Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm: C.S. Bruells , et al.; Sci. Rep. 11, 6302 (2021), Abstract
- Inhibition of Calpain Alleviates Apoptosis in Coxsackievirus B3-induced Acute Virus Myocarditis Through Suppressing Endoplasmic Reticulum Stress: H. Shi, et al.; Int. Heart J. 62, 900 (2021), Abstract
- New In Vitro Cellular Model for Molecular Studies of Retinitis Pigmentosa.: Huang, L., Marigo, V., et al.; Int. J. Mol. Sci. 22, (2021), Application(s): WB / Reactant(s): Mouse, Abstract
- N-Acetyl-L-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice.: Sarkar, C., Lipinski, M. M., et al.; Sci. Rep. 11, 9249 (2021), Application(s): WB / Reactant(s): Mouse, Abstract
- Post-stroke dendritic arbor regrowth – a cortical repair process requiring the actin nucleator Cobl: Frahm, C., Qualmann, B., et al.; bioRxiv , (2021), Application(s): WB / Reactant(s): Mouse
- Poststroke dendritic arbor regrowth requires the actin nucleator Cobl.: Witte, O. W., Frahm, C., et al.; PLoS Biol. 19, e3001399 (2021), Application(s): WB / Reactant(s): Mouse, Abstract
- PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia: Rodríguez-Pascau, L., Britti, E., et al.; Neurobiol. Dis. 148, 105162 (2021), Abstract
- Mithramycin selectively attenuates DNA-damage-induced neuronal cell death: Makarevich, O., Sabirzhanov, B., et al.; Cell Death Dis. 11, 587 (2020), Abstract
- CaMKII/calpain interaction mediates ischemia/reperfusion injury in isolated rat hearts.: Lu, H. T., Feng, R. Q., et al.; Cell Death Dis. 11, 388 (2020), Reactant(s): Rat, Abstract
- The cell-permeable mitochondrial calcium uniporter inhibitor Ru265 preserves cortical neuron respiration after lethal oxygen glucose deprivation and reduces hypoxic/ischemic brain injury.: Robertson, G. S., Wilson, J. J., et al.; J. Cereb. Blood Flow Metab. 40, 1172 (2020), Reactant(s): Mouse, Abstract
- Collapsin Response Mediator Protein 4 (CRMP4) Facilitates Wallerian Degeneration and Axon Regeneration following Sciatic Nerve Injury.: Barker, P. A., Rambaldi, I., et al.; eNeuro 7, (2020), Application(s): WB, Abstract
- Screening of tau protein kinase inhibitors in a tauopathy-relevant cell-based model of tau hyperphosphorylation and oligomerization: Yadikar, H., Torres, I., et al.; PLoS One 15, e0224952 (2020), Abstract
- Calpain system is altered in survival motor neuron-reduced cells from in vitro and in vivo spinal muscular atrophy models: S. de la Fuente, et al.; Cell Death Dis. 11, 487 (2020), Abstract — Full Text
- Irradiation-Induced Upregulation of miR-711 Inhibits DNA Repair and Promotes Neurodegeneration Pathways: Sabirzhanov, B., Makarevich, O., et al.; Int. J. Mol. Sci. 21, (2020), Abstract
- Down-Regulation of miR-23a-3p Mediates Irradiation-Induced Neuronal Apoptosis: Sabirzhanov, B., Makarevich, O., et al.; Int. J. Mol. Sci. 21, (2020), Abstract
- Administration of all-trans retinoic acid after experimental traumatic brain injury is brain protective: Hummel, R., Ulbrich, S., et al.; Br. J. Pharmacol. 177, 5208 (2020), Abstract
- Activation of Cytosolic Calpain, Not Caspase, Is Underlying Mechanism for Hypoxic RGC Damage in Human Retinal Explants: M. Kobayashi-Otsugu, et al.; Invest. Ophthalmol. Vis. Sci. 61, 13 (2020), Abstract — Full Text
- Sex hormones modulate pathogenic processes in experimental traumatic brain injury: Gölz, C., Kirchhoff, F. P., et al.; J. Neurochem. 150, 173 (2019), Abstract
- N-acetyl-L-leucine treatment attenuates neuronal cell death and suppresses neuroinflammation after traumatic brain injury in mice: Sarkar, C., Hegdekar, N., et al.; bioRxiv , (2019), Application(s): WB / Reactant(s): Mouse
- cPLA2 activation contributes to lysosomal defects leading to impairment of autophagy after spinal cord injury.: Li, Y., Jones, J. W., et al.; Cell Death Dis. 10, 531 (2019), Application(s): WB / Reactant(s): Mouse, Abstract
- Novel Peptidomic Approach for Identification of Low and High Molecular Weight Tauopathy Peptides Following Calpain Digestion, and Primary Culture Neurotoxic Challenges.: Yang, Z., Wang, K. K., et al.; Int. J. Mol. Sci. 20, (2019), Application(s): WB / Reactant(s): Mouse, Abstract
- Inhibition of microRNA-711 limits angiopoietin-1 and Akt changes, tissue damage, and motor dysfunction after contusive spinal cord injury in mice.: Wu, J., Stoica, B. A., et al.; Cell Death Dis. 10, 839 (2019), Application(s): WB / Reactant(s): Mouse, Abstract
- Buffering of cytosolic calcium plays a neuroprotective role by preserving the autophagy-lysosome pathway during MPP+-induced neuronal death: S. Jung, et al.; Cell Death Dis. 5, 130 (2019), Application(s): ICC-IF / Reactant(s) Mouse, Abstract — Full Text
- Depletion of regulatory T cells increases T cell brain infiltration, reactive astrogliosis, and interferon-γ gene expression in acute experimental traumatic brain injury: T.J. Kramer, et al.; J. Neuroinflammation 16, 163 (2019), Abstract — Full Text
- MicroRNA-711-Induced Downregulation of Angiopoietin-1 Mediates Neuronal Cell Death: Sabirzhanov, B., Faden, A. I., et al.; J. Neurotrauma 35, 2462 (2018), Abstract
- Comparing effects of CDK inhibition and E2F1/2 ablation on neuronal cell death pathways in vitro and after traumatic brain injury: Aubrecht, T. G., Faden, A. I., et al.; Cell Death Dis. 9, 1121 (2018), Abstract
- A role for proteolytic regulation of δ-catenin in remodeling a subpopulation of dendritic spines in the rodent brain.: Yuan, L., Singh, D., et al.; J. Biol. Chem. 293, 11625 (2018), Application(s): WB / Reactant(s): Mouse, Abstract
- Lysosomal damage after spinal cord injury causes accumulation of RIPK1 and RIPK3 proteins and potentiation of necroptosis.: Liu, S., Li, Y., et al.; Cell Death Dis. 9, 476 (2018), Application(s): WB / Reactant(s): Mouse, Abstract
- BrainPhys® increases neurofilament levels in CNS cultures, and facilitates investigation of axonal damage after a mechanical stretch-injury in vitro: T.C. Jackson, et al.; Exp Neurol. 300, 232 (2018), Abstract
- Calpain inhibition ameliorates scald burn-induced acute lung injury in rats: P. Du, et al.; Burns Trauma 6, 28 (2018), Abstract — Full Text
- Exposure to mild blast forces induces neuropathological effects, neurophysiological deficits and biochemical changes: A. Hernandez, et al.; Mol. Brain 11, 64 (2018), Reactant(s) Rat, Abstract — Full Text
- Cerebrospinal Fluid Biomarkers Are Associated With Glial Fibrillary Acidic Protein and αII-spectrin Breakdown Products in Brain Tissues Following Penetrating Ballistic-Like Brain Injury in Rats: K.E. DeDominicis, et al.; Front. Neurol. 9, 490 (2018), Application(s): WB / Reactant(s) Rat, Abstract — Full Text
- Neuroprotective Effects of Psalmotoxin-1, an Acid-Sensing Ion Channel (ASIC) Inhibitor, in Ischemia Reperfusion in Mouse Eyes: A. Dibas, et al.; Curr. Eye Res. 43, 921 (2018), Abstract
- Chemosensitivity of U251 Cells to the Co-treatment of D-Penicillamine and Copper: Possible Implications on Wilson Disease Patients: M. Katerji, et al.; Front. Mol. Neurosci. 10, 10 (2017), Abstract — Full Text
- Contribution of Calpain and Caspases to Cell Death in Cultured Monkey RPE Cells: E. Nakajima, et al.; Invest. Ophthalmol. Vis. Sci. 58, 5412 (2017), Abstract — Full Text
- Mild fluid percussion injury induces diffuse axonal damage and reactive synaptic plasticity in the mouse olfactory bulb: M.A. Powell, et al.; Neuroscience 371, 106 (2017), Application(s): Western Blot, Abstract
- Sequestosome 1 Deficiency Delays, but Does Not Prevent Brain Damage Formation Following Acute Brain Injury in Adult Mice: A. Sebastiani, et al.; Front. Neurosci. 11, 678 (2017), Application(s): WB / Reactant(s) Mouse, Abstract — Full Text
- Impaired autophagosome clearance contributes to neuronal death in a piglet model of neonatal hypoxic-ischemic encephalopathy.: Jiang, W., Sun, D., et al.; Cell Death Dis. 8, e2919 (2017), Application(s): WB / Reactant(s): Mouse, Abstract
- In Vitro Neurotoxicity Resulting from Exposure of Cultured Neural Cells to Several Types of Nanoparticles.: Larner, S. F., Xin, M., et al.; J. Cell Death 10, 1179670717694523 (2017), Application(s): WB, Abstract
- miR-711 upregulation induces neuronal cell death after traumatic brain injury: B. Sabirzhanov, et al.; Cell Death Differ. 23, 654 (2016), Application(s): Western Blot, Abstract
- Tissue Plasminogen Activator Neurotoxicity is Neutralized by Recombinant ADAMTS 13: M. Fan, et al.; Sci. Rep. 6, 25971 (2016), Application(s): Western blot, Abstract — Full Text
- Ammonium accumulation is a primary effect of 2-methylcitrate exposure in an in vitro model for brain damage in methylmalonic aciduria: H.P. Cudré-Cung, et al.; Mol. Genet. Metab. 119, 57 (2016), Application(s): Western blot analysis, Abstract
- Influence of weaning methods on the diaphragm after mechanical ventilation in a rat model: C.S. Bruells, et al.; BMC Pulm. Med. 16, 127 (2016), Application(s): Proteolysis, Calpain and caspase-3 activity measurement, Abstract — Full Text
- Calpain-mediated cleavage of collapsin response mediator protein-2 drives acute axonal degeneration.: Bähr, M., Urlaub, H., et al.; Sci. Rep. 6, 37050 (2016), Application(s): WB / Reactant(s): Rat, Abstract
- The Blockade of Transmembrane Cl Flux Mitigates I/R-Induced Heart Injury via the Inhibition of Calpain Activity: J. Y. Zhang, et al.; Cell. Physiol. Biochem. 35, 2121 (2015), Application(s): Western Blot, Abstract — Full Text
- Calpain-mediated cleavage of DARPP-32 in Alzheimer’s disease: K. Cho, et al.; Aging Cell 14, 878 (2015), Application(s): Western Blot, Abstract — Full Text
- Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.: Wu, J., Liu, S., et al.; Cell Death Dis. 6, e1582 (2015), Application(s): WB / Reactant(s): Rat, Abstract
- The nuclear splicing factor RNA binding motif 5 promotes caspase activation in human neuronal cells, and increases after traumatic brain injury in mice: T.C. Jackson, et al.; J. Cereb. Blood Flow Metab. 35, 655 (2015), Application(s): Western Blotting, Abstract
- Impaired autophagy flux is associated with neuronal cell death after traumatic brain injury.: Aungst, S., Faden, A. I., et al.; Autophagy 10, 2208 (2014), Application(s): WB / Reactant(s): Mouse, Abstract
- Allele-specific suppression of mutant huntingtin using antisense oligonucleotides: providing a therapeutic option for all Huntington disease patients.: Kordasiewicz, H., Bennett, C. F., et al.; PLoS One 9, e107434 (2014), Application(s): WB, Abstract
- Downregulation of miR-23a and miR-27a following experimental traumatic brain injury induces neuronal cell death through activation of proapoptotic Bcl-2 proteins.: Wu, J., Stoica, B. A., et al.; J. Neurosci. 34, 10055 (2014), Application(s): WB / Reactant(s): Mouse, Abstract
- Alpha II Spectrin breakdown products in immature Sprague Dawley rat hippocampus and cortex after traumatic brain injury.: Yang, Z., Schober, M. E., et al.; Brain Res. 1574, 105 (2014), Application(s): WB / Reactant(s): Mouse, Abstract
- Dual vulnerability of TDP-43 to calpain and caspase-3 proteolysis after neurotoxic conditions and traumatic brain injury.: Yang, Z., Wang, K. K., et al.; J. Cereb. Blood Flow Metab. 34, 1444 (2014), Application(s): WB / Reactant(s): Human, Abstract
- Live imaging and single-cell analysis reveal differential dynamics of autophagy and apoptosis.: Yuan, J., Xu, Y., et al.; Autophagy 9, 1418 (2013), Application(s): WB, Abstract
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