产品: DFNA5/GSDME 抗体 - N-terminal
货号: AF4016
描述: Rabbit polyclonal antibody to DFNA5/GSDME - N-terminal
应用: WB
反应: Human, Mouse
分子量: 30kDa; 55kD(Calculated).
蛋白号: O60443

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产品描述

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

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse
克隆:
Polyclonal
特异性:
DFNA5/GSDME Antibody detects N-terminal fragment of DFNA5/GSDME.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
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.
别名:

展开/折叠

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;

抗原和靶标

免疫原:

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

Uniprot:
基因/基因ID:
表达:
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.

序列:
MFAKATRNFLREVDADGDLIAVSNLNDSDKLQLLSLVTKKKRFWCWQRPKYQFLSLTLGDVLIEDQFPSPVVVESDFVKYEGKFANHVSGTLETALGKVKLNLGGSSRVESQSSFGTLRKQEVDLQQLIRDSAERTINLRNPVLQQVLEGRNEVLCVLTQKITTMQKCVISEHMQVEEKCGGIVGIQTKTVQVSATEDGNVTKDSNVVLEIPAATTIAYGVIELYVKLDGQFEFCLLRGKQGGFENKKRIDSVYLDPLVFREFAFIDMPDAAHGISSQDGPLSVLKQATLLLERNFHPFAELPEPQQTALSDIFQAVLFDDELLMVLEPVCDDLVSGLSPTVAVLGELKPRQQQDLVAFLQLVGCSLQGGCPGPEDAGSKQLFMTAYFLVSALAEMPDSAAALLGTCCKLQIIPTLCHLLRALSDDGVSDLEDPTLTPLKDTERFGIVQRLFASADISLERLKSSVKAVILKDSKVFPLLLCITLNGLCALGREHS

翻译修饰 - O60443 作为底物

Site PTM Type Enzyme
K4 Ubiquitination
T6 Phosphorylation
Y80 Phosphorylation
K83 Ubiquitination
K98 Ubiquitination
K100 Ubiquitination
S106 Phosphorylation
T117 Phosphorylation
S132 Phosphorylation
C156 S-Nitrosylation
K248 Ubiquitination
S252 Phosphorylation
Y254 Phosphorylation
K286 Ubiquitination
K440 Ubiquitination
K467 Ubiquitination

研究背景

功能:

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.

翻译修饰:

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

细胞定位:

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
组织特异性:

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

亚基结构:

The N-terminal moiety forms homooligomer; disulfide-linked. May form an 16-mer complex. Oligomerization occurs in the presence of membranes.

蛋白家族:

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.

文献引用

1). 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 

2). 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]

3). 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=5.2]

4). Pharmacological inhibition of cGAS ameliorates postoperative cognitive dysfunction by suppressing caspase-3/GSDME-dependent pyroptosis. Neurochemistry international, 2024 (PubMed: 38843953) [IF=4.2]

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