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MABS1987

Sigma-Aldrich

Anti-SREBP-1 Antibody, clone 20B12

clone 20B12, from rabbit

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Synonym(s):
Sterol regulatory element-binding protein 1, SREBP-1, Sterol regulatory element-binding transcription factor 1
eCl@ss:
32160702

biological source

rabbit

Quality Level

antibody form

unpurified

antibody product type

primary antibodies

clone

20B12, monoclonal

species reactivity

human

species reactivity (predicted by homology)

mouse (based on 100% sequence homology)

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

ambient

target post-translational modification

unmodified

Gene Information

human ... SREBF1(6720)

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MABS2034ABS1508SAB4502850
vibrant-m

MABS2034

Anti-SREBP-1 Antibody, clone 2A4

vibrant-m

ABS1508

Anti-SREBP-1

Gene Information

human ... SREBF1(6720)

Gene Information

human ... SREBF1(6720)

Gene Information

human ... SREBF1(6720)

Gene Information

human ... SREBF1(6720)

species reactivity

human

species reactivity

hamster, canine, human

species reactivity

human

species reactivity

human, rat

biological source

rabbit

biological source

mouse

biological source

rabbit

biological source

rabbit

clone

20B12, monoclonal

clone

2A4, monoclonal

clone

polyclonal

clone

polyclonal

shipped in

ambient

shipped in

-

shipped in

ambient

shipped in

wet ice

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General description

Sterol regulatory element-binding protein 1 (UniProt: Q9WTN3; also known as SREBP-1, Sterol regulatory element-binding transcription factor 1) is encoded by the Srebf1 (also known as Srebp1) gene (Gene ID: 20787) in murine species. SREBPs are a family of transcription factors that regulate lipid homeostasis by controlling the expression of a range of enzymes that are required for endogenous cholesterol, fatty acid, triacylglyceride, and phospholipid synthesis. The three SREBP isoforms known as, SREBP-1a, SREBP-1c, and SREBP-2, have different roles in lipid synthesis. It has been reported that SREBP-1c is mainly involved in fatty acid synthesis and insulin induced glucose metabolism. SREBP-2 is mainly involved in cholesterol synthesis. SREBP-1a isoform is reported to be involved in both of these pathways. Isoform SREBP-1A predominates in spleen, while isoform IC predominates in liver, adrenal gland, brain and adipose tissue and both IA and IC are found in kidney, thymus, testis, muscle, jejunum, and ileum. Expression of SREBP-1C in the liver is reported to be controlled in a circadian manner with a peak at ZT16. SREBPs are synthetized as inactive precursor proteins that are bound to the endoplasmic reticulum membranes and upon activation, the precursor is cleaved off in a two-step process to release the N-terminal active domain in the nucleus. Sterols are shown to inhibit the cleavage of the precursor protein and the mature nuclear form is rapidly catabolized, thereby reducing transcription. SREBP-1 binds to the sterol regulatory element-1 (SRE1 5′-ATCACCCCAC-3′), which flanks the low density lipoprotein receptor gene and some genes involved in sterol biosynthesis. Mice overexpressing processed isoform SREBP-1A in adipocytes show enlarged white and brown adipocytes, increased rate of fatty acid synthesis and secretion leading to a fatty liver. Mice lacking isoform SREBP-1C show a lack of up-regulation of several lipogenic enzymes in response to high insulin or LXR activation. (Ref.: Eberle, D et al. (2004) Biochimie 86(11); 839-48).

Specificity

Clone 20B12 recognizes SREBP-1 in multiple human tissues.

Immunogen

His-tagged recombinant fragment corresponding to 219 amino acids from the N-terminal region of murine sterol regulatory element-binding protein 1.

Application

Anti-SREBP-1, clone 20B12, Cat. No. MABS1987, a rabbit monoclonal antibody, detects SREBP-1 in human tissues by Western Blotting.
Research Category
Signaling
Western Blotting Analysis: A 1:1,000 dilution from a representative lot detected SREBP-1 in 10 µg of HEK293 cell lysates.

Quality

Evaluated by Western Blotting in HepG2 cell lysates.

Western Blotting Analysis: A 1:1,000 dilution of this antibody detected SREBP-1 in 10 µg of HepG2 cell lysates.

Target description

~120 kDa observed; 120.54 kDa calculated. Uncharacterized bands may be observed in some lysate(s).

Physical form

Format: Unpurified
Rabbit monoclonal antibody in cell culture supernatant without azide.
Unpurified

Storage and Stability

Stable for 1 year at -20°C from date of receipt. Handling Recommendations: Upon receipt and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.

Other Notes

Concentration: Please refer to lot specific datasheet.

Disclaimer

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.

Storage Class

10 - Combustible liquids

wgk_germany

WGK 1


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Hong Lu et al.
Lipids in health and disease, 21(1), 46-46 (2022-05-26)
Hepatocyte nuclear factor 4α (HNF4α) and glucocorticoid receptor (GR), master regulators of liver metabolism, are down-regulated in fatty liver diseases. The present study aimed to elucidate the role of down-regulation of HNF4α and GR in fatty liver and hyperlipidemia. Adult
MiSung Kim et al.
JCI insight, 2(24) (2017-12-22)
Increased sugar consumption is a risk factor for the metabolic syndrome including obesity, hypertriglyceridemia, insulin resistance, diabetes, and nonalcoholic fatty liver disease (NAFLD). Carbohydrate responsive element-binding protein (ChREBP) is a transcription factor that responds to sugar consumption to regulate adaptive
Junhee Park et al.
Nature communications, 13(1), 5594-5594 (2022-09-24)
Insulin receptor (IR) signaling defects cause a variety of metabolic diseases including diabetes. Moreover, inherited mutations of the IR cause severe insulin resistance, leading to early morbidity and mortality with limited therapeutic options. A previously reported selective IR agonist without
Antwi-Boasiako Oteng et al.
Molecular nutrition & food research, 63(19), e1900385-e1900385 (2019-07-22)
The mechanisms underlying the deleterious effects of trans fatty acids on plasma cholesterol and non-alcoholic fatty liver disease (NAFLD) are unclear. Here, the aim is to investigate the molecular mechanisms of action of industrial trans fatty acids. Hepa1-6 hepatoma cells
Arturo Mendoza et al.
Science signaling, 14(709), eabh3839-eabh3839 (2021-11-17)
[Figure: see text].

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