Antibody data
- Antibody Data
- Antigen structure
- References [5]
- Comments [0]
- Validations
- Western blot [2]
- ELISA [1]
- Immunohistochemistry [1]
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- Product number
- ABIN396498 - Provider product page
- Provider
- antibodies-online
- Product name
- anti-Achalasia, Adrenocortical Insufficiency, Alacrimia (AAAS) (AA 1-101) antibody
- Antibody type
- Monoclonal
- Description
- This antibody is purified through a protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS.
- Reactivity
- Human, Mouse, Rat
- Host
- Mouse
- Epitope
- AA 1-101
- Isotype
- IgG
- Antibody clone number
- 5A1
- Vial size
- 100 μg
- Storage
- Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles
Submitted references Two Italian patients with novel AAAS gene mutation expand allelic and phenotypic spectrum of triple A (Allgrove) syndrome.
The transmembrane nucleoporin NDC1 is required for targeting of ALADIN to nuclear pore complexes.
Tissue-specific expression and subcellular localization of ALADIN, the absence of which causes human triple A syndrome.
Deficiency of ferritin heavy-chain nuclear import in triple a syndrome implies nuclear oxidative damage as the primary disease mechanism.
The nuclear pore complex protein ALADIN is anchored via NDC1 but not via POM121 and GP210 in the nuclear envelope.
Palka C, Giuliani R, Brancati F, Mohn A, Di Muzio A, Calabrese O, Huebner A, De Grandis D, Chiarelli F, Ferlini A, Stuppia L
Clinical genetics 2010 Mar;77(3):298-301
Clinical genetics 2010 Mar;77(3):298-301
The transmembrane nucleoporin NDC1 is required for targeting of ALADIN to nuclear pore complexes.
Yamazumi Y, Kamiya A, Nishida A, Nishihara A, Iemura S, Natsume T, Akiyama T
Biochemical and biophysical research communications 2009 Nov 6;389(1):100-4
Biochemical and biophysical research communications 2009 Nov 6;389(1):100-4
Tissue-specific expression and subcellular localization of ALADIN, the absence of which causes human triple A syndrome.
Cho AR, Yang KJ, Bae Y, Bahk YY, Kim E, Lee H, Kim JK, Park W, Rhim H, Choi SY, Imanaka T, Moon S, Yoon J, Yoon SK
Experimental & molecular medicine 2009 Jun 30;41(6):381-6
Experimental & molecular medicine 2009 Jun 30;41(6):381-6
Deficiency of ferritin heavy-chain nuclear import in triple a syndrome implies nuclear oxidative damage as the primary disease mechanism.
Storr HL, Kind B, Parfitt DA, Chapple JP, Lorenz M, Koehler K, Huebner A, Clark AJ
Molecular endocrinology (Baltimore, Md.) 2009 Dec;23(12):2086-94
Molecular endocrinology (Baltimore, Md.) 2009 Dec;23(12):2086-94
The nuclear pore complex protein ALADIN is anchored via NDC1 but not via POM121 and GP210 in the nuclear envelope.
Kind B, Koehler K, Lorenz M, Huebner A
Biochemical and biophysical research communications 2009 Dec 11;390(2):205-10
Biochemical and biophysical research communications 2009 Dec 11;390(2):205-10
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Supportive validation
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- Experimental details
- WB
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- WB
Supportive validation
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- ELISA
Supportive validation
- Submitted by
- antibodies-online (provider)
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- Experimental details
- IHC