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Merck
CN

SAB2102992

Anti-SREBF1, (N-terminal) antibody produced in rabbit

affinity isolated antibody

别名:

Anti-SREBP1

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
MDL number:
Conjugate:
unconjugated
Clone:
polyclonal
Application:
western blot
Species reactivity:
dog, mouse, goat, horse, rabbit, human, guinea pig, rat
Citations:
2
Technique(s):
western blot: suitable
Uniprot accession no.:
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产品名称

Anti-SREBF1, (N-terminal) antibody produced in rabbit, affinity isolated antibody

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

mol wt

125 kDa

species reactivity

dog, mouse, goat, horse, rabbit, human, guinea pig, rat

packaging

pkg of 100 μL buffered aqueous solution
pkg of 50 μg lyophilized powder

concentration

0.5 mg - 1 mg/mL

technique(s)

western blot: suitable

NCBI accession no.

UniProt accession no.

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... SREBF1(6720)

Biochem/physiol Actions

SREBF1is a transcription factor that binds to the sterol regulatory element-1 (SRE1), which is a decamer flanking the low density lipoprotein receptor gene and some genes involved in sterol biosynthesis. The protein is synthesized as a precursor that is attached to the nuclear membrane and endoplasmic reticulum. Following cleavage, the mature protein translocates to the nucleus and activates transcription by binding to the SRE1. Sterols inhibit the cleavage of the precursor, and the mature nuclear form is rapidly catabolized, thereby reducing transcription. The protein is a member of the basic helix-loop-helix-leucine zipper (bHLH-Zip) transcription factor family. This gene is located within the Smith-Magenis syndrome region on chromosome 17.This gene encodes a transcription factor that binds to the sterol regulatory element-1 (SRE1), which is a decamer flanking the low density lipoprotein receptor gene and some genes involved in sterol biosynthesis. The protein is synthesized as a precursor that is attached to the nuclear membrane and endoplasmic reticulum. Following cleavage, the mature protein translocates to the nucleus and activates transcription by binding to the SRE1. Sterols inhibit the cleavage of the precursor, and the mature nuclear form is rapidly catabolized, thereby reducing transcription. The protein is a member of the basic helix-loop-helix-leucine zipper (bHLH-Zip) transcription factor family. This gene is located within the Smith-Magenis syndrome region on chromosome 17. Two transcript variants encoding different isoforms have been found for this gene.

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.

Immunogen

Synthetic peptide directed towards the N terminal region of human SREBF1

Other Notes

Synthetic peptide located within the following region: AGRGRANGLDAPRAGADRGAMDCTFEDMLQLINNQDSDFPGLFDPPYAGS

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存储类别

10 - Combustible liquids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

常规特殊物品
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历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Anhua Lin et al.
Journal of diabetes investigation, 14(10), 1160-1171 (2023-07-07)
High glucose increases the accumulation of lipid droplets in hepatocytes, which eventually results in nonalcoholic fatty liver disease in patients with diabetes. However, the specific mechanism or communication between adipocyte and hepatocyte lipid metabolism is still ambiguous. In this study
Ethan David Cohen et al.
JCI insight, 6(5) (2021-01-29)
Preterm birth increases the risk for pulmonary hypertension and heart failure in adulthood. Oxygen therapy can damage the immature cardiopulmonary system and may be partially responsible for the cardiovascular disease in adults born preterm. We previously showed that exposing newborn

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