Product: DFNA5/GSDME Antibody - N-terminal
Catalog: AF4016
Description: Rabbit polyclonal antibody to DFNA5/GSDME - N-terminal
Application: WB
Cited expt.: WB
Reactivity: Human, Mouse
Mol.Wt.: 30kDa; 55kD(Calculated).
Uniprot: O60443

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Product Info

Source:
Rabbit IgG
Application:
WB 1:500-1:2000
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse
Clonality:
Polyclonal
Specificity:
DFNA5/GSDME Antibody detects N-terminal fragment of DFNA5/GSDME.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

2310037D07Rik; 4932441K13Rik; Deafness, autosomal dominant 5; Deafness, autosomal dominant 5 protein; DFNA5; DFNA5 gene; DFNA5_HUMAN; Dfna5h; EG14210; Fin15; ICERE 1; ICERE-1; Inversely correlated with estrogen receptor expression 1; Non-syndromic hearing impairment protein 5; Nonsyndromic hearing impairment protein; Gasdermin-E;GSDME_HUMAN;ICERE1;

Immunogens

Immunogen:

A synthesized peptide derived from human DFNA5(Accession O60443), corresponding to N-terminal amino acid.

Uniprot:
Gene(ID):
Expression:
O60443 GSDME_HUMAN:

Expressed in cochlea. Low level of expression in heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas, with highest expression in placenta.

Sequence:
MFAKATRNFLREVDADGDLIAVSNLNDSDKLQLLSLVTKKKRFWCWQRPKYQFLSLTLGDVLIEDQFPSPVVVESDFVKYEGKFANHVSGTLETALGKVKLNLGGSSRVESQSSFGTLRKQEVDLQQLIRDSAERTINLRNPVLQQVLEGRNEVLCVLTQKITTMQKCVISEHMQVEEKCGGIVGIQTKTVQVSATEDGNVTKDSNVVLEIPAATTIAYGVIELYVKLDGQFEFCLLRGKQGGFENKKRIDSVYLDPLVFREFAFIDMPDAAHGISSQDGPLSVLKQATLLLERNFHPFAELPEPQQTALSDIFQAVLFDDELLMVLEPVCDDLVSGLSPTVAVLGELKPRQQQDLVAFLQLVGCSLQGGCPGPEDAGSKQLFMTAYFLVSALAEMPDSAAALLGTCCKLQIIPTLCHLLRALSDDGVSDLEDPTLTPLKDTERFGIVQRLFASADISLERLKSSVKAVILKDSKVFPLLLCITLNGLCALGREHS

Research Backgrounds

Function:

Plays a role in the TP53-regulated cellular response to DNA damage probably by cooperating with TP53.

Switches CASP3-mediated apoptosis induced by TNF or danger signals, such as chemotherapy drugs, to pyroptosis. Produced by the cleavage of GSDME by CASP3, perforates cell membrane and thereby induces pyroptosis. After cleavage, moves to the plasma membrane where it strongly binds to inner leaflet lipids, bisphosphorylated phosphatidylinositols, such as phosphatidylinositol (4,5)-bisphosphate. Mediates secondary necrosis downstream of the mitochondrial apoptotic pathway and CASP3 activation as well as in response to viral agents. Exhibits bactericidal activity.

PTMs:

Cleavage at Asp-270 by CASP3 (mature and uncleaved precursor forms) relieves autoinhibition and is sufficient to initiate pyroptosis.

Subcellular Location:

Cell membrane.

Cytoplasm>Cytosol.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Expressed in cochlea. Low level of expression in heart, brain, placenta, lung, liver, skeletal muscle, kidney and pancreas, with highest expression in placenta.

Family&Domains:

Intramolecular interactions between N- and C-terminal domains may be important for autoinhibition in the absence of activation signal. The intrinsic pyroptosis-inducing activity is carried by the N-terminal domain, that is released upon cleavage by CASP3.

Belongs to the gasdermin family.

References

1). PLGA confers upon conventional nonfluorescent molecules luminescent properties to trigger 1O2-induced pyroptosis and immune response in tumors. Journal of nanobiotechnology, 2025 (PubMed: 39844156) [IF=10.2]

2). Iron induces B cell pyroptosis through Tom20–Bax–caspase–gasdermin E signaling to promote inflammation post-spinal cord injury. Journal of Neuroinflammation, 2023 (PubMed: 37480037) [IF=9.3]

Application: WB    Species: Mouse    Sample: B cells

Fig. 3 Pyroptosis induced by iron accumulation may occur in splenic B cells after SCI. a Three days after SCI, serum samples were collected for quantification of the protein expression levels of MCP-1, IL-1β, IL-6, and TNF-α by ELISA. b Three days after SCI, injured spinal cord homogenates were collected for quantification of the protein expression levels of MCP-1, IL-1β, IL-6, and TNF-α by ELISA. c Three days after SCI, the spleen was stained with Prussian blue to detect the level of iron ion. d Three days after SCI, serum samples were collected to quantify the concentration of iron ions. e Three days after SCI, B cell lysates were collected to quantify the concentration of iron ions. f Detection of Tom20-Bax-caspase-GSDME pathway-related protein expression in B cells by western blot. g The knock-down efficiency of AAV on Tom20 in B cells was verified. h, l, m The expression levels of MCP-1, IL-1 β, IL-6, TNF- α, IgG and IgM in serum of different groups were detected by ELISA. i–k Three days after SCI, the spleens of mice were observed, and the spleen length and organ index of different groups were compared. n, o, q The spleen was taken for HE staining, Prussian blue staining, and immunofluorescence. CD19+ was red, dapi was blue, and merge was combined. p Detection of nerve evoked potentials in different groups of mice. r Detection of the expression of Tom20-Bax-caspsae-GSDME pathway-related proteins in different groups of B cells. All data are expressed as the mean ± SD (n ≥ 3 replicates per group). ns P > 0.05, * P 

3). Neuronal-specific TNFAIP1 ablation attenuates postoperative cognitive dysfunction via targeting SNAP25 for K48-linked ubiquitination. Cell communication and signaling : CCS, 2023 (PubMed: 38102610) [IF=8.4]

4). Neuroprotection of celastrol against postoperative cognitive dysfunction through dampening cGAS-STING signaling. Experimental neurology, 2024 (PubMed: 39369806) [IF=4.6]

5). Liproxstatin‑1 induces cell cycle arrest, apoptosis, and caspase‑3/GSDME‑dependent secondary pyroptosis in K562 cells. International Journal of Oncology, 2022 (PubMed: 36004469) [IF=4.5]

6). Pharmacological inhibition of cGAS ameliorates postoperative cognitive dysfunction by suppressing caspase-3/GSDME-dependent pyroptosis. Neurochemistry international, 2024 (PubMed: 38843953) [IF=4.4]

7). Pyropheophorbide-α methyl ester-mediated photodynamic therapy triggers pyroptosis in osteosarcoma cells via the ROS/caspase-3/GSDME pathway. Photodiagnosis and photodynamic therapy, 2024 (PubMed: 39615558) [IF=3.1]

8). Maresin1 alleviates neuroinflammation by inhibiting caspase-3/ GSDME-mediated pyroptosis in mice cerebral ischemia-reperfusion model. Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association, 2024 (PubMed: 38782167) [IF=2.0]

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