製品: DFNA5/GSDME Antibody - N-terminal
カタログ: AF4016
タンパク質の説明: Rabbit polyclonal antibody to DFNA5/GSDME - N-terminal
アプリケーション: WB
反応性: Human, Mouse
分子量: 30kDa; 55kD(Calculated).
ユニプロット: O60443

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製品説明

ソース:
Rabbit IgG
アプリケーション:
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.

反応性:
Human,Mouse
クローナリティ:
Polyclonal
特異性:
DFNA5/GSDME Antibody detects N-terminal fragment of DFNA5/GSDME.
コンジュゲート:
Unconjugated.
精製:
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.
別名:

折りたたみ/展開

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;

免疫原

免疫原:

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

Uniprot:
遺伝子(ID):
発現特異性:
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.

タンパク質配列:
MFAKATRNFLREVDADGDLIAVSNLNDSDKLQLLSLVTKKKRFWCWQRPKYQFLSLTLGDVLIEDQFPSPVVVESDFVKYEGKFANHVSGTLETALGKVKLNLGGSSRVESQSSFGTLRKQEVDLQQLIRDSAERTINLRNPVLQQVLEGRNEVLCVLTQKITTMQKCVISEHMQVEEKCGGIVGIQTKTVQVSATEDGNVTKDSNVVLEIPAATTIAYGVIELYVKLDGQFEFCLLRGKQGGFENKKRIDSVYLDPLVFREFAFIDMPDAAHGISSQDGPLSVLKQATLLLERNFHPFAELPEPQQTALSDIFQAVLFDDELLMVLEPVCDDLVSGLSPTVAVLGELKPRQQQDLVAFLQLVGCSLQGGCPGPEDAGSKQLFMTAYFLVSALAEMPDSAAALLGTCCKLQIIPTLCHLLRALSDDGVSDLEDPTLTPLKDTERFGIVQRLFASADISLERLKSSVKAVILKDSKVFPLLLCITLNGLCALGREHS

PTMs - O60443 基板として

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

機能:

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.

PTMs:

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

細胞の位置付け:

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
組織特異性:

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

サブユニット構造:

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

タンパク質ファミリー:

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.

参考文献

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). 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]

Application: WB    Species: Human    Sample: K562 cells

Figure 6 - Lip-1 induces pyroptosis in K562 leukemia cells via caspase-3/GSDME activation. K562 cells were treated with 10 and 20 µM Lip-1 for 24 h in most experiments; part F shows an experiment in which K562 cells were pretreated with z-DEVD-FMK for 3 h and further treated with 20 µM Lip-1 for 12 h. (A) K562 cells double-stained with Annexin V-FITC/PI for flow cytometry. (B) Expression levels of TNF-α assessed by real-time polymerase chain reaction and normalized to RPLP0. (C) Protein levels of TNF-α in cell culture supernatants and cell lysates detected by enzyme-linked immunosorbent assay (minimum detectable concentration, 6.9 pg/ml). (D) BAX, cleaved caspase-3, and cleaved PARP protein levels quantified by western blotting. (E) Lip-1 induced caspase-3, but not caspase-1, activation in a concentrationand time-dependent manner. Caspase-1/-3 activities were measured by colorimetric assay. (F) Comparison of cell viability and the protein level of N-terminal GSDME in Lip-1-treated K562 cells and the effects of z-DEVD-FMK inhibition. SH-SY5Y whole cell lysate was used as a positive control. (G) Expression levels of GSDME assessed by real-time polymerase chain reaction and normalized to RPLP0. (H) GSDME and cleaved N-terminal GSDME protein levels quantified by western blotting. SH-SY5Y whole cell lysate was used as a positive control. (I) TUNEL assay used to determine DNA fragmentation. Specimens treated with DNase Ⅰ were used as positive controls. Data represent the mean ± SD from at least three independent experiments. *P<0.05, **P<0.01 and ***P<0.001 vs. Control. Lip-1, liproxstatin-1; ns, not significant.

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