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SREBF1

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All listed services and products are For Research Use Only. Do Not use in any diagnostic or therapeutic applications.

Background

Sterol regulatory element binding transcription factor 1(SREBF1, also known as SREBP1) is an endoplasmic reticulum anchored precursor transcription factor encoded by SREBF1 gene. After protein shearing, it can form an active nuclear subtype, which is widely expressed in liver, adipose tissue and proliferating tumor cells. Unlike SREBF2, which mainly regulates cholesterol synthesis, mature SREBF1 activated by nucleus can specifically bind to sterol response elements (SREs), and target the transcription and expression of gene clusters related to fatty acid and triglyceride synthesis. In the physiological state of sterol deficiency, SREBF1 can enter the nucleus through proteolytic shearing, start the physiological lipid synthesis process, and provide sufficient lipid raw materials for cell membrane structure synthesis. However, under the pathological state of insulin stimulation or malignant transformation of cells, SREBF1 will be continuously overactivated, which will drive the abnormal de novo synthesis of lipids and provide material support for the rapid division and proliferation of tumor cells. Compared with conventional housekeeping transcription factors, SREBF1 has a unique function of specifically regulating fatty acid synthesis, and can not be compensated by other SREBP family subtypes. The loss of SREBF1 function can significantly inhibit the expression of lipid synthesis gene and block the proliferation of tumor cells; However, the sustained over-activation of this molecule will induce fatty degeneration of liver and accelerate the malignant progress of tumor, which is the core target of lipid transcription regulation mechanism research and metabolic anti-tumor drug screening.

SREBF1 realizes sterol sensing and transcription regulation through the shear transport cycle of endoplasmic reticulum-nucleus, and specifically recognizes and binds the downstream SRE nucleic acid sequence by relying on the conserved basic helix-loop-helix leucine zipper (bHLH-LZ) domain. Its unique DNA binding motif clearly distinguishes its function of targeting fatty acid metabolism from SREBF2, which regulates cholesterol metabolism, and forms a lipid regulation pathway with specific functions. SREBF1-mediated transcription cascade can link the sterol sensing signal with the cytoplasmic lipid synthesis and metabolism pathway, and dynamically regulate the lipid synthesis flux according to the nutritional status of the body and the signal of cell proliferation. This transcription factor is widely involved in many key physiological and pathological processes, such as adipocyte differentiation, liver lipid homeostasis maintenance and tumor cell metabolic reprogramming. Deficient SREBF1 signaling abolishes baseline fatty acid synthesis capacity. Therefore, SREBF1 represents a pivotal research target for lipogenic transcription study and metabolic compound screening.

Fig. 1 Full regulatory model of SREBF1 lipogenic transcriptional axis for tumor lipid metabolism research reagents. (OA Literature)Fig. 1 Schematic diagram of SREBP-1 protein structure, sterol-dependent maturation cascade and oncogenic upstream signaling network.1

SREBF1 Protein Function: Core Roles in Lipogenic Transcription and Metabolic Tuning

The biological functions of SREBF1 are focused on SRE DNA binding and fatty acid gene transactivation:

  • Sterol Response Element Binding: Recognizes promoter SRE motifs via bHLH-LZ domain to initiate transcription.
  • Lipogenic Gene Activation: Upregulates FASN, ACC, SCD1 fatty acid synthase target genes.
  • Lipid Homeostasis Maintenance: Sustains basal membrane lipid synthesis under nutrient-balanced cells.
  • Tumor Metabolism Modulation: Boosts de novo lipogenesis to sustain cancer cell proliferation.
  • Disease Relevance: SREBF1 overexpression causes fatty liver and tumor growth; knockout inhibits lipogenic oncogenic signaling.

SREBF1 Protein Product

Creative Biolabs offers high-quality SREBF1 full-length precursor and mature nuclear isoform proteins, including isolated bHLH-LZ DNA-binding domain variants. These products retain native SRE DNA binding and transcriptional cofactor interaction activity, suitable for lipogenic transcriptional screening assays. All SREBF1 proteins undergo strict quality control to ensure consistent performance and reliable application across diverse research platforms.

SREBF1 Protein Product

Not finding the membrane protein product you need? Contact us to start your one-stop custom service!

SREBF1 Stable Cell Line Product

Creative Biolabs provides custom-engineered SREBF stable cell lines, including overexpression and blank control models. These cell lines are optimized for lipogenic transcription profiling and fatty acid metabolic signal functional analysis. Each cell line undergoes stringent validation to ensure stable expression profiles and consistent functional performance in diverse experimental contexts.

SREBF1 Stable Cell Line Product

Not finding the stable cell line product you need? Contact us to start your one-stop custom service!

SREBF1 Recombinant Antibody Product

High-specificity recombinant antibodies targeting SREBF1 are developed via advanced antibody engineering technologies, with no cross-reactivity with SREBF2 paralogs. These antibodies are validated for ER membrane and nuclear dual localization detection and liver/tumor tissue expression profiling, and can be combined with FASN detection reagents to analyze lipogenic transcriptional complexes in metabolic cell models.

SREBF1 Recombinant Antibody Product

Not finding the recombinant antibody product you need? Contact us to start your one-stop custom service!

Product Features

  • Native SRE DNA Binding & Cofactor Interaction Activity: Preserves intact lipogenic transcriptional capacity for lipid metabolism research.
  • SREBF1 Specificity: Eliminates non-specific cross-recognition of cholesterol-regulating SREBF2.
  • Metabolic Oncology Compatibility: Optimized reagent series for fatty liver and lipogenic tumor therapeutic screening workflows.
  • Comprehensive Customization Support: Facilitates end-to-end development of customized proteins, antibodies and stable cell lines to address lipogenic transcription research demands.

Custom SREBF1 Research Services

Beyond catalog products, Creative Biolabs offers specialized custom services for SREBF1 research:

  • Custom SREBF1 Protein Production: Tailored expression of mutant and tagged SREBF1 constructs for SRE promoter binding analysis.
  • Custom Antibody Development: Generation of SREBF1-specific antibodies for ER/nuclear immunostaining.
  • Stable Cell Line Engineering: Construction of SREBF1-modified cell models for lipogenic signaling research.
  • Functional Assay Development: Custom design of transcriptional reporter and lipid synthesis detection workflows.

Frequently Asked Questions (FAQ)

  1. What is the primary function of SREBF1?

    A1: SREBF1 is an ER-derived transcription factor that enters nucleus to bind SRE sequences and activate fatty acid synthesis target genes.

  2. Why is SREBF1 a significant research target?

    A2: SREBF1 acts as master switch of de novo lipogenesis, driving hepatic steatosis and cancer metabolic reprogramming.

  3. Are Creative Biolabs' SREBF1 products suitable for clinical use?

    A3: No, all SREBF1 products and services are strictly for research use only, not intended for clinical diagnosis or treatment.

  4. What types of SREBF1 products does Creative Biolabs offer?

    A4: Offerings include full-length/pre-cleaved SREBF1 proteins, isoform-specific detection antibodies and custom stable cell lines for lipid transcription research.

  5. How are SREBF1 proteins validated for activity?

    A5: SREBF1 proteins are validated via SRE promoter DNA binding and lipogenic gene transactivation functional testing.

Reference
  1. Zhao, Qiushi, Xingyu Lin, and Guan Wang. "Targeting SREBP-1-mediated lipogenesis as potential strategies for cancer." Frontiers in oncology 12 (2022): 952371. Under Open Access license CC BY 4.0, without modification. https://doi.org/10.3389/fonc.2022.952371
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