TBEV gE

Tick-Borne Encephalitis Virus gE Recombinant

This recombinant protein is derived from E. coli and contains the Tick-borne Encephalitis Virus glycoprotein E regions, specifically amino acids 95-229.
Shipped with Ice Packs
Cat. No.
BT7008
Source
Escherichia Coli.

TBEV gE C-end

Tick-Borne Encephalitis Virus gE C-end Recombinant

This recombinant protein is derived from E. coli and contains the C-terminal region of the Tick-borne Encephalitis Virus glycoprotein E, specifically amino acids 296-414.
Shipped with Ice Packs
Cat. No.
BT7099
Source
Escherichia Coli.

TBEV gE middle

Tick-Borne Encephalitis Virus gE Middle Recombinant

This recombinant protein, derived from E. coli, contains the middle region (amino acids 50-250) of the Tick-borne Encephalitis Virus glycoprotein E.
Shipped with Ice Packs
Cat. No.
BT7188
Source
Escherichia Coli.
Appearance
Sterile Filtered clear solution.

TBEV NE

Tick-Borne Encephalitis Virus NE Recombinant

This recombinant protein, derived from E. coli, has a molecular weight of 37 kDa and contains the N-terminus regions of the Tick-borne encephalitis virus glycoprotein E.
Shipped with Ice Packs
Cat. No.
BT7280

Encephalitis Japanese 12kda

Japanese Encephalitis Virus 12kda Recombinant

Recombinant Japanese Encephalitis Virus, produced in E. coli, consists of 110 amino acids with a molecular weight of 12kDa. The protein features an N-terminal His tag and undergoes purification using a proprietary chromatographic method.
Shipped with Ice Packs
Cat. No.
BT6700
Source
Escherichia Coli.
Appearance
Sterile Filtered clear solution.

JEV

Japanese Encephalitis Virus ENV Recombinant

This recombinant protein, derived from E. coli, encompasses the full-length Japanese Encephalitis virus ENV antigen, exhibiting a molecular weight of 50 kDa. It is engineered with a 6-histidine tag. GenBank Accession Number: AHK05344.1
Shipped with Ice Packs
Cat. No.
BT6824
Source
Escherichia Coli.

TBEV Core

Tick-Borne Encephalitis Virus Core Protein Recombinant

This recombinant protein, derived from E. coli, contains epitopes of the Tick-borne Encephalitis Virus core protein.
Shipped with Ice Packs
Cat. No.
BT6900
Source
Escherichia Coli.

TBEV NS3

Tick-Borne Encephalitis Virus NS3 Recombinant

This recombinant protein, derived from E. coli, contains epitopes of the Tick-borne Encephalitis Virus NS3 protein.
Shipped with Ice Packs
Cat. No.
BT7351
Source
Escherichia Coli.

TBEV preM

Tick-Borne Encephalitis Virus preM Recombinant

This recombinant protein is derived from E. coli and contains the Tick-borne Encephalitis Virus preM protein epitopes.
Shipped with Ice Packs
Cat. No.
BT7414
Source
Escherichia Coli.
Definition and Classification

Encephalitis is an inflammation of the brain tissue, often caused by viral infections, but can also result from bacterial infections, autoimmune diseases, or other inflammatory conditions. It is classified into two main types:

  • Primary Encephalitis: Direct infection of the brain by a virus or other pathogen.
  • Secondary Encephalitis: An immune-mediated response following an infection elsewhere in the body.
Biological Properties

Key Biological Properties:

  • Inflammatory Response: Characterized by the infiltration of immune cells into the brain tissue.
  • Cytokine Production: Elevated levels of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α).

Expression Patterns:

  • Viral Encephalitis: High expression of viral antigens in infected neurons and glial cells.
  • Autoimmune Encephalitis: Presence of autoantibodies targeting neuronal surface proteins.

Tissue Distribution:

  • Localized: Infections can be localized to specific brain regions.
  • Diffuse: Inflammation can spread throughout the brain.
Biological Functions

Primary Biological Functions:

  • Immune Response Activation: Encephalitis triggers the activation of both innate and adaptive immune responses.
  • Pathogen Recognition: Involves pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) that detect pathogen-associated molecular patterns (PAMPs).

Role in Immune Responses:

  • Innate Immunity: Rapid response involving microglia and astrocytes.
  • Adaptive Immunity: Activation of T cells and B cells, leading to the production of antibodies.
Modes of Action

Mechanisms with Other Molecules and Cells:

  • Cytokine Signaling: Cytokines released by infected cells recruit immune cells to the site of infection.
  • Cell-Cell Interactions: Direct interactions between infected neurons and immune cells.

Binding Partners:

  • Viral Proteins: Bind to specific receptors on host cells to facilitate entry.
  • Autoantibodies: Bind to neuronal surface proteins, disrupting normal function.

Downstream Signaling Cascades:

  • NF-κB Pathway: Activation leads to the production of pro-inflammatory cytokines.
  • JAK-STAT Pathway: Involved in the signaling of various cytokines and growth factors.
Regulatory Mechanisms

Transcriptional Regulation:

  • Transcription Factors: NF-κB and IRF3 play key roles in the transcription of inflammatory genes.
  • Epigenetic Modifications: DNA methylation and histone modifications can influence gene expression.

Post-Translational Modifications:

  • Phosphorylation: Modifies the activity of signaling proteins.
  • Ubiquitination: Targets proteins for degradation, regulating their levels and activity.
Applications

Biomedical Research:

  • Model Systems: Animal models are used to study the pathogenesis and treatment of encephalitis.
  • Biomarker Discovery: Identifying biomarkers for early diagnosis and monitoring disease progression.

Diagnostic Tools:

  • Imaging Techniques: MRI and CT scans to detect brain inflammation.
  • Molecular Diagnostics: PCR and serological tests to identify causative pathogens.

Therapeutic Strategies:

  • Antiviral Therapies: Target specific viral infections causing encephalitis.
  • Immunomodulatory Treatments: Corticosteroids and intravenous immunoglobulins to reduce inflammation.
Role in the Life Cycle

Development:

  • Pediatric Encephalitis: Can affect brain development in children, leading to long-term neurological deficits.

Aging:

  • Neurodegeneration: Chronic inflammation may contribute to neurodegenerative diseases such as Alzheimer’s.

Disease:

  • Acute Encephalitis: Rapid onset with severe symptoms, requiring immediate medical attention.
  • Chronic Encephalitis: Persistent inflammation leading to progressive neurological decline.

Encephalitis remains a complex and multifaceted condition, with ongoing research aimed at better understanding its mechanisms and developing effective treatments.

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