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Product Info

ELISA 1:10000, WB 1:500-1:2000, IHC 1:200-1:1000
*The optimal dilutions should be determined by the end user.

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.

Monoclonal [AFB1817]
ALDH1A1 antibody detects endogenous levels of total ALDH1A1.
Cite Format: Affinity Biosciences Cat# BF0220, RRID:AB_2833841.
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


Acetaldehyde dehydrogenase 1; AHD2; AL1A1_HUMAN; ALDC; Aldehyde dehydrogenase 1 family member A1; Aldehyde dehydrogenase 1 soluble; Aldehyde dehydrogenase 1A1; Aldehyde dehydrogenase; Aldehyde dehydrogenase cytosolic; Aldehyde dehydrogenase family 1 member A1; Aldehyde dehydrogenase liver cytosolic; ALDH 1; ALDH 1A1; ALDH class 1; ALDH, liver cytosolic; ALDH-E1; ALDH1 A1; ALDH1; ALDH11; ALDH1A1; ALHDII; cytosolic; epididymis luminal protein 12; epididymis luminal protein 9; epididymis secretory sperm binding protein Li 53e; HEL-S-53e; MGC2318; PUMB1; RALDH 1; RalDH1; Retinal dehydrogenase 1;



Purified recombinant fragment of human ALDH1A1 expressed in E. Coli.

ALDH1A1 is an aldehyde dehydrogenase able to oxidize a wide variety of aliphatic aldehydes (retinaldehyde, acetaldehyde, etc.) to the corresponding carboxylic acids (retinoic acid, acetic acid, etc.). ALDH1A1 (also known as RALDH1, ALDH1, or AHD2) is highly expressed in the dorsal retina, ventral midbrain (dopaminergic neurons), and hematopoietic stem cells. ALDH1A1 is involved in retinoic acid (RA) synthesis during vertebrate embryogenesis. ALDH1A1 is first detected at E9.0-E10.5 in cranial tissues (ventral mesencephalon, dorsal retina, thymic primordia, optic vesicles) and in the mesonephros.

PTMs - P00352 As Substrate

Site PTM Type Enzyme
S2 Acetylation
S2 Phosphorylation
T6 Phosphorylation
K22 Acetylation
K65 Acetylation
R68 Methylation
R85 Methylation
K91 Acetylation
T105 Phosphorylation
Y119 Phosphorylation
K128 Acetylation
K128 Ubiquitination
K139 Acetylation
K139 Ubiquitination
T144 Phosphorylation
Y154 Phosphorylation
K252 Acetylation
T267 Phosphorylation
S314 Phosphorylation
Y316 Phosphorylation
T337 Phosphorylation
T341 Phosphorylation
K353 Acetylation
S360 Phosphorylation
K362 Acetylation
K367 Acetylation
K398 Ubiquitination
K410 Acetylation
K412 Acetylation
K412 Ubiquitination
S413 Phosphorylation
K419 Acetylation
T424 Phosphorylation
Y426 Phosphorylation
S429 Phosphorylation
K435 Acetylation
K435 Ubiquitination
T442 Phosphorylation
Y481 Phosphorylation
Y486 Phosphorylation
K490 Ubiquitination
T493 Phosphorylation
K495 Acetylation
K495 Ubiquitination

Research Backgrounds


Can convert/oxidize retinaldehyde to retinoic acid. Binds free retinal and cellular retinol-binding protein-bound retinal (By similarity). May have a broader specificity and oxidize other aldehydes in vivo.


The N-terminus is blocked most probably by acetylation.

Subcellular Location:


Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:



Belongs to the aldehyde dehydrogenase family.

Research Fields

· Metabolism > Metabolism of cofactors and vitamins > Retinol metabolism.

· Metabolism > Global and overview maps > Metabolic pathways.


1). Huang R et al. CCL5 derived from tumor-associated macrophages promotes prostate cancer stem cells and metastasis via activating β-catenin/STAT3 signaling. Cell Death & Disease 2020 Apr 16;11(4):234 (PubMed: 32300100) [IF=9.0]

Application: IHC    Species: human    Sample: prostate cancer cells

Fig. 7 The clinical significance of CCL5 in predicting prostate cancer prognosis. a The CCL5 mRNA expression differences between different tissues or different groups of prostate cancer patients. CCL5 expression increased in prostate cancer tumor tissues when compared with nonmalignant prostate tissues. Castration-resistant prostate cancer patients exhibited increased CCL5 expression when compared with patients with good prognosis. Metastatic prostate tumors exhibited increased CCL5 expression when compared with primary prostate tumors. The following datasets were analyzed including GSE6919 (n = 93), GSE21034 (n = 179), GSE37199 (n = 106), and GSE46691 (n = 545). b Enrichment analysis indicated that CCL5 was positively correlated with stem cell-related genes. c There were significant positive correlations between the expression levels of CCL5 and stemness-related genes including CD133 and STAT3 (n = 93). d High CCL5 expression in prostate cancer patients predicted poor overall survival (n = 82) and poor progression-free survival (n = 34). e A commercialized prostate tissue microarray containing 90 prostate cancer tissues and 90 para-carcinoma tissues was analyzed. Prostate cancer patients with high Gleason grade exhibited increased CCL5 expression (p < 0.05). CCL5 overexpression was observed in prostate cancer tissues when compared with para-carcinoma tissues (p < 0.05). There were significant positive correlations between CCL5 and PCSCs-related proteins including ALDH1A1 and STAT3 (n = 180) in the samples of human prostate cancer tissue microarray. Scale bar, 100 μm.

2). Wang S et al. XIAOPI formula inhibits breast cancer stem cells via suppressing TAMs/CXCL1 pathway. Frontiers in Pharmacology 2019 Nov 15;10:1371. (PubMed: 31803057) [IF=5.6]

Application: IF/ICC    Species: mouse    Sample: 4T1-Luc xenografts

FIGURE 5 | XIAOPI formula (XPS) suppresses breast tumor growth and breast cancer stem cells (CSCs) activity in vivo. (D–E) XPS administration significantly decreased the infiltration degree of macrophages as well as their M2 phenotype polarization and C-X-C motif chemokine ligand 1 (CXCL1) expression in the 4T1-Luc xenografts in vivo. n = 3. (F–G) XPS administration significantly decreased the proportions of ALDH+ subpopulations (F) and suppressed the expression levels of ALDH1A1 (G) in the 4T1-Luc xenografts in vivo. n = 3. Scale bar = 20 μm. All values are presented as the mean ± SD, **P < 0.05.

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For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.