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Mouse Anti-ALAS2 Recombinant Antibody (V2-180597) (CBMAB-A2133-YC)

Provided herein is a Mouse monoclonal antibody against Human 5'-Aminolevulinate Synthase 2. The antibody can be used for immunoassay techniques, such as WB.
See all ALAS2 antibodies
Published Data
Mouse Anti-ALAS2 Recombinant Antibody (6C1) in WB
SFXN4 depletion reduces hemoglobinization by destabilizing ferrochelatase (FECH) and by promoting translational inhibition of ALAS2. (A) Hemoglobin in differentiated K562 (Scramble/SFXN4 KO) cell at 3 and 6 days post induction of differentiation with sodium butyrate. (B) Image of cell pellets 6 days post induction of differentiation with sodium butyrate. (C) Western blot of SFXN4, ALAS2 and FECH from K562 (Scramble/SFXN4 KO) cells. (D) Western blot of ALAS2 in differentiated K562 (Scramble/CRISPR clone) cells at different time points. Means and standard deviations of quantified data from three independent experiments are shown under the blot. (E) Quantification of ALAS2 mRNA in scramble and SFXN4 knockout cells at 0, 3, and 6 days after sodium butyrate. Images are representative of three independent experiments. ...View More
Paul, B. T., Tesfay, L., Winkler, C. R., Torti, F. M., & Torti, S. V. (2019). Sideroflexin 4 affects Fe-S cluster biogenesis, iron metabolism, mitochondrial respiration and heme biosynthetic enzymes. Scientific Reports, 9(1), 19634.
Mouse Anti-ALAS2 Recombinant Antibody (6C1) in WB
Validation of the expression of ALAS2, c-Kit, and miR-221/222 during emodin induction of K562 cells. a Real-time PCR analysis of c-Kit mRNA expression during emodin-induced K562 cell erythroid differentiation. b Real-time PCR analysis of ALAS2 mRNA during emodin-induced K562 cell erythroid differentiation. c Western blot analysis of c-Kit and ALAS2 proteins during emodin induction of K562 cells. d Real-time PCR analysis of miR-221 expression during emodin induction. e Real-time PCR analysis of miR-222 expression during emodin induction of K562 cells. ...View More
Ma, Y. N., Chen, M. T., Wu, Z. K., Zhao, H. L., Yu, H. C., Yu, J., & Zhang, J. W. (2013). Emodin can induce K562 cells to erythroid differentiation and improve the expression of globin genes. Molecular and cellular biochemistry, 382, 127-136.
Mouse Anti-ALAS2 Recombinant Antibody (6C1) in WB
Regulation of ALAS2 gene expression by HIF1. (A) Real-time PCR assay of HIF1A and ALAS2 mRNA levels in K562 cells transfected with the HIF1R expression plasmid (pHIF1R) or empty plasmid (pcDNA) and subsequently incubated under hypoxia for 24 h. (B) Real-time PCR assay of HIF1A and ALAS2 mRNA levels in K562 cells that were transfected with the HIF1R interference vector (pSiHIF1R) or pSilencer control (pSiCON) and subsequently incubated under hypoxia for 24 h. (C) Real-time PCR assay of HIF1A and ALAS2 mRNA levels in K562 cells transfected with siRNA targeted to HIF1A (siHIF1R) or siRNA control (siCON). After transfection for 24 h, the transfection medium was replaced with complete medium and the cells were cultured under hypoxia for an additional 24 h. The asterisk indicates a p value of <0.01. (D) Western blotting assay of HIF1R and ALAS2 protein levels in K562 cells transfected with the HIF1R expression plasmid or corresponding empty vector and subsequently incubated under hypoxia for 48 h. (E) Western blotting assay of HIF1R and ALAS2 protein levels in K562 cells transfected with the HIF1R interference plasmid or the corresponding empty vector and subsequently incubated under hypoxia for 48 h. (F) Western blotting assay of ALAS2 protein levels in K562 cells transfected with siRNA targeting HIF1A mRNA or an siRNA control. After transfection for 24 h, the transfection medium was replaced with complete medium and the cells were cultured under hypoxia for an additional 24 h. ...View More
Zhang, F. L., Shen, G. M., Liu, X. L., Wang, F., Zhao, H. L., Yu, J., & Zhang, J. W. (2011). Hypoxic induction of human erythroid-specific δ-aminolevulinate synthase mediated by hypoxia-inducible factor 1. Biochemistry, 50(7), 1194-1202.

Summary

Host Animal
Mouse
Specificity
Human
Clone
V2-180597
Antibody Isotype
IgG2a, κ
Application
WB, ELISA

Basic Information

Immunogen
ALAS2 (NP_000023, 1 a.a. ~ 100 a.a) partial recombinant protein with GST tag.
Host Species
Mouse
Specificity
Human
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4
Preservative
None
Concentration
Batch dependent
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
5'-Aminolevulinate Synthase 2
Introduction
ALAS2 specifies an erythroid-specific mitochondrially located enzyme. The encoded protein catalyzes the first step in the heme biosynthetic pathway. Defects in this gene cause X-linked pyridoxine-responsive sideroblastic anemia.
Entrez Gene ID
212
UniProt ID
P22557
Alternative Names
5'-Aminolevulinate Synthase 2; 5-Aminolevulinate Synthase 2; Aminolevulinate, Delta-, Synthase 2; Delta-Aminolevulinate Synthase 2; 5-Aminolevulinic Acid Synthase 2; Delta-ALA Synthase 2; EC 2.3.1.37; ALAS-E; ALASE; ASB;
Biological Process
Cellular iron ion homeostasis Source: UniProtKB
Erythrocyte development Source: GO_Central
Erythrocyte differentiation Source: UniProtKB
Heme biosynthetic process Source: UniProtKB
Hemoglobin biosynthetic process Source: UniProtKB
Oxygen homeostasis Source: UniProtKB
Protoporphyrinogen IX biosynthetic process Source: UniProtKB-UniPathway
Response to hypoxia Source: UniProtKB
Cellular Location
Mitochondrion matrix
Involvement in disease
Anemia, sideroblastic, 1 (SIDBA1): A form of sideroblastic anemia that shows a variable hematologic response to pharmacologic doses of pyridoxine. Sideroblastic anemia is characterized by anemia of varying severity, hypochromic peripheral erythrocytes, systemic iron overload secondary to chronic ineffective erythropoiesis, and the presence of bone marrow ringed sideroblasts. Sideroblasts are characterized by iron-loaded mitochondria clustered around the nucleus.
Erythropoietic protoporphyria, X-linked dominant (XLDPT): The disease is caused by variants affecting the gene represented in this entry. Gain of function mutations in ALS2 are responsible for XLDPT, but they can also be a possible aggravating factor in congenital erythropoietic porphyria and other erythropoietic disorders caused by mutations in other genes (PubMed:21309041). A form of porphyria. Porphyrias are inherited defects in the biosynthesis of heme, resulting in the accumulation and increased excretion of porphyrins or porphyrin precursors. They are classified as erythropoietic or hepatic, depending on whether the enzyme deficiency occurs in red blood cells or in the liver. XLDPT is characterized biochemically by a high proportion of zinc-protoporphyrin in erythrocytes, in which a mismatch between protoporphyrin production and the heme requirement of differentiating erythroid cells leads to overproduction of protoporphyrin in amounts sufficient to cause photosensitivity and liver disease.
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For research use only. Not intended for any clinical use.

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