추천 제품
생물학적 소스
mouse
Quality Level
항체 형태
ascites fluid
항체 생산 유형
primary antibodies
클론
2AL-1D6, monoclonal
종 반응성
human
제조업체/상표
Chemicon®
기술
ELISA: suitable
immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable
동형
IgG1
NCBI 수납 번호
UniProt 수납 번호
배송 상태
dry ice
타겟 번역 후 변형
unmodified
유전자 정보
human ... ABCD1(215)
특이성
Human ALDP. No cross reactivity with mouse ALDRP, PMP70. Cross reactivity to an unidentified 80 kD MW protein is present in lymphoblastoid cells, but not in several other cells or tissues tested. MAB2164 can be used to analyze ALDP protein in cells and tissues from normal individuals, or from patients with adrenoleukodystrophy (ALD) or Zellweger syndrome and related peroxisomal diseases, and provides an excellent marker for peroxisomes (Mosser et al. 1994). About 70% of ALD male patients have no detectable ALDP in fibroblasts or leukocytes. A similar proportion of carrier females may show mosaïcism for the presence or absence of ALDP.
면역원
ALDP1 fragment from aa 279 to 482 as a fusion protein
Epitope: a.a. 279-482
애플리케이션
Detect Adrenoleukodystrophy Protein using this Anti-Adrenoleukodystrophy Protein Antibody, a.a. 279-482, clone 2AL-1D6 validated for use in ELISA, WB, IC, IH.
ELISA: 1:500-1:5,000
Immunoblotting: 1:500-1:5,000
Immunohistochemistry: 1:500-1:5,000
Immunocytochemistry: 1:500-1:5,000
Optimal working dilutions must be determined by the end user.
Immunoblotting: 1:500-1:5,000
Immunohistochemistry: 1:500-1:5,000
Immunocytochemistry: 1:500-1:5,000
Optimal working dilutions must be determined by the end user.
Research Category
Neuroscience
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Neurodegenerative Diseases
물리적 형태
Ascites. Liquid, does not contain any preservative.
저장 및 안정성
Maintain at -20°C in undiluted aliquots up to 12 months. Avoid repeated freeze/thaw cycles.
법적 정보
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
면책조항
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
nwg
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
M Contreras et al.
Archives of biochemistry and biophysics, 334(2), 369-379 (1996-10-15)
Adrenoleukodystrophy (X-ALD) is a demyelinating disorder characterized by the accumulation of saturated very-long-chain fatty acids (> C22:0) due to the impaired activity of lignoceroyl-CoA ligase. The gene responsible for the disease was found to code for a 84-kDa peroxisomal integral
Miguel Agustin Contreras et al.
Archives of biochemistry and biophysics, 477(2), 211-218 (2008-07-08)
Krabbe disease is a neuroinflammatory disorder in which galactosylsphingosine (psychosine) accumulates in nervous tissue. To gain insight into whether the psychosine-induced effects in nervous tissue extend to peripheral organs, we investigated the expression of cytokines and their effects on peroxisomal
Stefan Schönberger et al.
Archives of neurology, 64(5), 651-657 (2007-03-14)
X-linked adrenoleukodystrophy (X-ALD) is the most common inherited peroxisomal disorder. It is caused by impaired function of ALD protein that results in accumulation of very long-chain fatty acids in tissues and body fluids. So far, hematopoietic stem cell transplantation (HSCT)
J Mosser et al.
Human molecular genetics, 3(2), 265-271 (1994-02-01)
Adrenoleukodystrophy is a severe genetic demyelinating disease associated with an impairment of beta-oxidation of very long chain fatty acids (VLCFA) in peroxisomes. Earlier studies had suggested that a deficiency in VLCFA CoA synthetase was the primary defect. A candidate adrenoleukodystrophy
X-linked adrenoleukodystrophy.
Aubourg, P and Mandel, J L
Annals of the New York Academy of Sciences, 804, 461-476 (1996)
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