Anti-brain lipid binding protein antibody abn14 anoxia at birth

100% performance guaranteed key spec table species reactivity

Key applications



Antibody type

M, H



Affinity purified

Polyclonal antibody


Catalogue number





Anti-brain lipid binding protein antibody

Alternate names

• brain lipid-binding protein

• fatty acid-binding protein 7

• mammary-derived growth inhibitor related

• brain lipid binding protein

• fatty acid binding protein 7, brain

• mammary-derived growth inhibitor-related

Background information

BLBP (brain lipid-binding protein) belongs to a family of small, highly conserved, cytoplasmic proteins that bind long-chain fatty acids and other hydrophobic ligands.

BLBPs play essential roles in fatty acid uptake, transport and metabolism.Anoxia at birth BLBP can be used as a molecular marker for radial glia (a major neural progenitor cell type and a scaffolding supporting neuronal migration) in the developing central nervous system. Radial glia play an essential role in the generation of the cerebral cortex through their function as neuronal precursors and as neuronal migration guides.


Product information


Affinity purified


• P1 mouse brain tissue lysate


Purified rabbit polyclonal in buffer containing 0.1 M tris-glycine (ph 7.4, 150 mm nacl) with 0.05% sodium azide.



Detect brain lipid binding protein using this anti-brain lipid binding protein antibody validated for use in WB, IH.

Key applications

anoxia at birth

• western blotting

• immunohistochemistry

Application notes

Immunohistochemistry analysis: A 1:300 dilution of ABN14 antibody from a previous lot detected brain lipid binding protein in mouse cerebellum tissue.

Biological information


GST-tagged recombinant protein corresponding to human brain lipid-binding protein.


Cytoplasmic domain


Please refer to the certificate of analysis for the lot-specific concentration.




This antibody recognizes brain lipid-binding protein.

Species reactivity

• mouse

• human

Species reactivity note

Proven to react with mouse. Predicted to react with human based on 100% sequence homology. Rat homology – 88%.

Antibody type

Polyclonal antibody

anoxia at birth

Entrez gene number

• NP_001437.1

Entrez gene summary

The protein encoded by this gene is a brain fatty acid binding protein. Fatty acid binding proteins (fabps) are a family of small, highly conserved, cytoplasmic proteins that bind long-chain fatty acids and other hydrophobic ligands. FABPs are thought to play roles in fatty acid uptake, transport, and metabolism. [provided by refseq].

Gene symbol






Purification method

Affinity purfied

UniProt number

• O15540

UniProt summary

FUNCTION: B-FABP could be involved in the transport of a so far unknown hydrophobic ligand with potential morphogenic activity during CNS development. It is required for the establishment of the radial glial fiber system in developing brain, a system that is necessary for the migration of immature neurons to establish cortical layers by similarity.Anoxia at birth


TISSUE SPECIFICITY: expressed in brain and other neural tissues.

DOMAIN: forms a beta-barrel structure that accommodates the hydrophobic ligand in its interior.

SEQUENCE SIMILARITIES: belongs to the calycin superfamily. Fatty-acid binding protein (FABP) family.

Molecular weight

~ 15 kda

Physicochemical information


Materials information

Toxicological information

Safety information according to GHS

Safety information

Product usage statements

Quality assurance

Evaluated by western blot in P1 mouse brain tissue lysate.

Western blot analysis: 0.01 µg/ml of this antibody detected brain lipid-binding protein in 10 µg of P1 mouse brain tissue lysate.

Usage statement

• 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.Anoxia at birth

Storage and shipping information

Storage conditions

Stable for 1 year at 2-8°C from date of receipt.

Packaging information

Material size

100 µg

Transport information

Supplemental information


There is growing evidence and a consensus in the field that most pediatric brain tumors originate from stem cells, of which radial glial cells constitute a subtype. Here we show that orthotopic transplantation of human radial glial (RG) cells to the subventricular zone of the 3rd ventricle–but not to other transplantation sites–of the brain in immunocompromised NOD-SCID mice, gives rise to tumors that have the hallmarks of CNS primitive neuroectodermal tumors (pnets). The resulting mouse model strikingly recapitulates the phenotype of pnets.Anoxia at birth importantly, the observed tumorigenic transformation was accompanied by aspects of an epithelial to mesenchymal transition (EMT)-like process. It is also noteworthy that the tumors are highly invasive, and that they effectively recruit mouse endothelial cells for angiogenesis. These results are significant for several reasons. First, they show that malignant transformation of radial glial cells can occur in the absence of specific mutations or inherited genomic alterations. Second, they demonstrate that the same radial glial cells may either give rise to brain tumors or differentiate normally depending upon the microenvironment of the specific region of the brain to which the cells are transplanted.Anoxia at birth in addition to providing a prospect for drug screening and development of new therapeutic strategies, the resulting mouse model of pnets offers an unprecedented opportunity to identify the cancer driving molecular alterations and the microenvironmental factors that are responsible for committing otherwise normal radial glial cells to a malignant phenotype.



Sox9 is critical for suppression of neurogenesis but not initiation of gliogenesis in the cerebellum.

Vong, KI; leung, CK; behringer, RR; kwan, KM

Molecular brain




Abstract anzeigen

The high mobility group (HMG) family transcription factor sox9 is critical for induction and maintenance of neural stem cell pool in the central nervous system (CNS).Anoxia at birth in the spinal cord and retina, sox9 is also the master regulator that defines glial fate choice by mediating the neurogenic-to-gliogenic fate switch. On the other hand, the genetic repertoire governing the maintenance and fate decision of neural progenitor pool in the cerebellum has remained elusive.By employing the cre/loxp strategy, we specifically inactivated sox9 in the mouse cerebellum. Unexpectedly, the self-renewal capacity and multipotency of neural progenitors at the cerebellar ventricular zone (VZ) were not perturbed upon sox9 ablation. Instead, the mutants exhibited an increased number of VZ-derived neurons including purkinje cells and gabaergic interneurons. Simultaneously, we observed continuous neurogenesis from sox9-null VZ at late gestation, when normally neurogenesis ceases to occur and gives way for gliogenesis.Anoxia at birth surprisingly, glial cell specification was not affected upon sox9 ablation.Our findings suggest sox9 may mediate the neurogenic-to-gliogenic fate switch in mouse cerebellum by modulating the termination of neurogenesis, and therefore indicate a functional discrepancy of sox9 between the development of cerebellum and other major neural tissues.


Activation of sonic hedgehog signaling in neural progenitor cells promotes glioma development in the zebrafish optic pathway.

Ju, B; chen, W; spitsbergen, JM; lu, J; vogel, P; peters, JL; wang, YD; orr, BA; wu, J; henson, HE; jia, S; parupalli, C; taylor, MR





Abstract anzeigen

Dysregulation of sonic hedgehog (shh) signaling has been implicated in glioma pathogenesis.Anoxia at birth yet, the role of this pathway in gliomagenesis remains controversial because of the lack of relevant animal models. Using the cytokeratin 5 promoter, we ectopically expressed a constitutively active zebrafish smoothened (smoa1) in neural progenitor cells and analyzed tumorigenic capacity of activated shh signaling in both transient and stable transgenic fish. Transient transgenic fish overexpressing smoa1 developed retinal and brain tumors, suggesting smoa1 is oncogenic in the zebrafish central nervous system (CNS). We further established stable transgenic lines that simultaneously developed optic pathway glioma (OPG) and various retinal tumors. In one of these lines, up to 80% of F1 and F2 fish developed tumors within 1 year of age.Anoxia at birth microarray analysis of tumor samples showed upregulated expression of genes involved in the cell cycle, cancer signaling and shh downstream targets ptc1, gli1 and gli2a. Tumors also exhibited specific gene signatures characteristic of radial glia and progenitor cells as transcriptions of radial glia genes cyp19a1b, s100β, blbp, gfap and the stem/progenitor genes nestin and sox2 were significantly upregulated. Overexpression of GFAP, s100β, BLBP and sox2 was confirmed by immunofluorescence. We also detected overexpression of mdm2 throughout the optic pathway in fish with OPG, therefore implicating the mdm2-tp53 pathway in glioma pathogenesis. In conclusion, we demonstrate that activated shh signaling initiates tumorigenesis in the zebrafish CNS and provide the first OPG model not associated with neurofibromatosis 1.Anoxia at birth


Loss of usp9x disrupts cortical architecture, hippocampal development and tgfβ-mediated axonogenesis.

Stegeman, S; jolly, LA; premarathne, S; gecz, J; richards, LJ; mackay-sim, A; wood, SA

PloS one




Abstract anzeigen

The deubiquitylating enzyme usp9x is highly expressed in the developing mouse brain, and increased usp9x expression enhances the self-renewal of neural progenitors in vitro. USP9X is a candidate gene for human neurodevelopmental disorders, including lissencephaly, epilepsy and X-linked intellectual disability. To determine if usp9x is critical to mammalian brain development we conditionally deleted the gene from neural progenitors, and their subsequent progeny. Mating usp9x(loxp/loxp) mice with mice expressing cre recombinase from the nestin promoter deleted usp9x throughout the entire brain, and resulted in early postnatal lethality.Anoxia at birth although the overall brain architecture was intact, loss of usp9x disrupted the cellular organization of the ventricular and sub-ventricular zones, and cortical plate. Usp9x absence also led to dramatic reductions in axonal length, in vivo and in vitro, which could in part be explained by a failure in tgf-β signaling. Deletion of usp9x from the dorsal telencephalon only, by mating with emx1-cre mice, was compatible with survival to adulthood but resulted in reduction or loss of the corpus callosum, a dramatic decrease in hippocampal size, and disorganization of the hippocampal CA3 region. This latter phenotypic aspect resembled that observed in doublecortin knock-out mice, which is an usp9x interacting protein.Anoxia at birth this study establishes that usp9x is critical for several aspects of CNS development, and suggests that its regulation of tgf-β signaling extends to neurons.


IKKβ/NF-κb disrupts adult hypothalamic neural stem cells to mediate a neurodegenerative mechanism of dietary obesity and pre-diabetes.

Li, J; tang, Y; cai, D

Nature cell biology




Abstract anzeigen

Adult neural stem cells (nscs) are known to exist in a few regions of the brain; however, the entity and physiological/disease relevance of adult hypothalamic nscs (htnscs) remain unclear. This work shows that adult htnscs are multipotent and predominantly present in the mediobasal hypothalamus of adult mice. Chronic high-fat-diet feeding led to not only depletion but also neurogenic impairment of htnscs associated with ikkβ/NF-κb activation.Anoxia at birth in vitro htnsc models demonstrated that their survival and neurogenesis markedly decreased on ikkβ/NF-κb activation but increased on ikkβ/NF-κb inhibition, mechanistically mediated by ikkβ/NF-κb-controlled apoptosis and notch signalling. Mouse studies revealed that htnsc-specific ikkβ/NF-κb activation led to depletion and impaired neuronal differentiation of htnscs, and ultimately the development of obesity and pre-diabetes. In conclusion, adult htnscs are important for the central regulation of metabolic physiology, and ikkβ/NF-κb-mediated impairment of adult htnscs is a critical neurodegenerative mechanism for obesity and related diabetes.



Apoptosis-inducing factor downregulation increased neuronal progenitor, but not stem cell, survival in the neonatal hippocampus after cerebral hypoxia-ischemia.Anoxia at birth

Sun, Y; zhang, Y; wang, X; blomgren, K; zhu, C

Molecular neurodegeneration




Abstract anzeigen

A considerable proportion of all newly generated cells in the hippocampus will die before becoming fully differentiated, both under normal and pathological circumstances. The caspase-independent apoptosis-inducing factor (AIF) has not been investigated previously in this context.Postnatal day 8 (P8) harlequin (hq) mutant mice, expressing lower levels of AIF, and wild type littermates were injected with brdu once daily for two days to label newborn cells. On P10 mice were subjected to hypoxia-ischemia (HI) and their brains were analyzed 4 h, 24 h or 4 weeks later. Overall tissue loss was 63.5% lower in hq mice 4 weeks after HI.Anoxia at birth short-term survival (4 h and 24 h) of labeled cells in the subgranular zone was neither affected by AIF downregulation, nor by HI. Long-term (4 weeks) survival of undifferentiated, BLBP-positive stem cells was reduced by half after HI, but this was not changed by AIF downregulation. Neurogenesis, however, as judged by brdu/neun double labeling, was reduced by half after HI in wild type mice but preserved in hq mice, indicating that primarily neural progenitors and neurons were protected. A wave of cell death started early after HI in the innermost layers of the granule cell layer (GCL) and moved outward, such that 24 h after HI dying cells could be detected in the entire GCL.These findings demonstrate that AIF downregulation provides not only long-term overall neuroprotection after HI, but also protects neural progenitor cells, thereby rescuing hippocampal neurogenesis.Anoxia at birth


Lithium reduced neural progenitor apoptosis in the hippocampus and ameliorated functional deficits after irradiation to the immature mouse brain.

Kaiming huo,yanyan sun,hongfu li,xiaonan du,xiaoyang wang,niklas karlsson,changlian zhu,klas blomgren

Molecular and cellular neurosciences



Abstract anzeigen

Lithium was recently shown to inhibit apoptosis and promote survival of neural progenitor cells after hypoxia-ischemia in the immature rat brain. Our aim was to evaluate the effects of lithium on cell death and proliferation in the hippocampus after irradiation (IR) to the immature brain. Male mice were injected with 2mmol/kg lithium chloride i.P. On postnatal day 9 (P9) and additional lithium injections, 1mmol/kg, were administered at 24h intervals for up to 7days.Anoxia at birth brdu was injected 4h after lithium injections on P9 and P10. The left hemisphere received a single dose of 8gy (MV photons) on P11. The animals were euthanized 6h or 7weeks after IR. The number of brdu-labeled cells in the subgranular zone (SGZ) of the granule cell layer (GCL) 6h after IR was 24% higher in the lithium-treated mice. The number of proliferating, phospho-histone H3-positive cells in the SGZ 7weeks after IR was 59% higher in the lithium group, so the effect was long-lasting. The number of apoptotic cells in the SGZ 6h after IR was lower in the lithium group, as judged by 3 different parameters, pyknosis, staining for active caspase-3 and TUNEL. Newly formed cells (brdu-labeled 1 or 2days before IR) showed the greatest degree of protection, as judged by 50% fewer TUNEL-positive cells, whereas non-brdu-labeled cells showed 38% fewer TUNEL-positive cells 6h after IR.Anoxia at birth consequently, the growth retardation of the GCL was less pronounced in the lithium group. The number and size of microglia in the DG were also lower in the lithium group, indicating reduced inflammation. Learning was facilitated after lithium treatment, as judged by improved context-dependent fear conditioning, and improved place learning, as judged by assessment in the intellicage platform. In summary, lithium administration could decrease IR-induced neural progenitor cell apoptosis in the GCL of the hippocampus and ameliorate learning impairments. It remains to be shown if lithium can be used to prevent the debilitating cognitive late effects seen in children treated with cranial radiotherapy.Anoxia at birth