Customize FKBP17-3 Antibody

Description

Clarification of Terminology

The term "FKBP17-3 Antibody" does not align with established nomenclature for FKBP family proteins or their corresponding antibodies. The FKBP family includes well-characterized members such as FKBP3, FKBP11, and FKBP12, each with distinct roles in immunoregulation, protein folding, and cellular signaling. No references to "FKBP17-3" exist in peer-reviewed literature, commercial antibody databases, or gene/protein repositories (e.g., GeneCards, UniProt).

Possible Interpretations:

Typographical Error: The correct term may be FKBP3 Antibody, a polyclonal antibody targeting FKBP3 (Q00688), which is well-documented in HIV latency studies.
Hypothetical Construct: If "FKBP17-3" refers to a novel antibody variant, no experimental data or validation exist in the provided sources.

FKBP3 Antibody: Characteristics and Applications

To address potential intent, we focus on FKBP3 Antibody, a validated research tool. Below are key details from peer-reviewed studies and commercial product specifications.

Biomatik Antibody (CAU22762)

Parameter	Detail
Host	Rabbit
Immunogen	Ala2~Asp224 (FKBP3)
Applications	WB, IHC, ICC, IP
Reactivity	Human
Purification	Antigen affinity purification
Concentration	Not specified
Storage	-20°C in PBS with 50% glycerol and 0.02% sodium azide

Proteintech Antibody (11755-1-AP)

Parameter	Detail
Host	Rabbit
Immunogen	FKBP3 fusion protein (Ag2351)
Applications	WB, IHC, IF/ICC, ELISA
Reactivity	Human, mouse, rat
Observed MW	25–30 kDa
RRID	AB_2102983

Role in HIV-1 Latency

FKBP3 facilitates HIV-1 latency by recruiting HDAC1/2 to the viral long terminal repeat (LTR), promoting histone deacetylation and transcriptional silencing .

Mechanism: FKBP3 binds YY1, which anchors the complex to the HIV-1 LTR.
Impact: FKBP3 knockout reactivates latent HIV-1 in cell lines (C11, J-Lat 10.6) and primary CD4+ T cells .

Interaction with Immunosuppressants

FKBP3 has higher affinity for rapamycin (IC50: ~1 nM) than FK506, making it a critical target for immunosuppressive therapies .

Antibody Validation

FKBP3 antibodies are validated for:

Western Blot: Detects 25–30 kDa bands in human, mouse, and rat lysates.
Immunoprecipitation: Co-IP of FKBP3 with YY1 and HDAC1/2 in HIV latency models .
Immunohistochemistry: Localization in plasma cells and lymphoid tissues .

Critical Analysis of Potential Misinterpretations

If "FKBP17-3" refers to a hypothetical antibody variant, key considerations include:

Target Specificity: FKBP family members share structural homology (e.g., FK domains), necessitating rigorous validation to avoid cross-reactivity.
Functional Relevance: Antibodies targeting FKBP3 are prioritized due to its role in HIV latency and immunosuppression, unlike less-studied FKBP isoforms.

Product Specs

Buffer

**Preservative:** 0.03% Proclin 300
**Constituents:** 50% Glycerol, 0.01M PBS, pH 7.4

Form

Liquid

Lead Time

Made-to-order (14-16 weeks)

Synonyms

FKBP17-3 antibody; At1g73655 antibody; F25P22.7Peptidyl-prolyl cis-trans isomerase FKBP17-3 antibody; chloroplastic antibody; PPIase FKBP17-3 antibody; EC 5.2.1.8 antibody; FK506-binding protein 17-3 antibody; AtFKBP17-3 antibody; Immunophilin FKBP17-3 antibody; Rotamase antibody

Target Names

FKBP17-3

Uniprot No.

Q8LB65

Target Background

Function

FKBP17-3 Antibody targets FKBP17-3, a protein that functions as a peptidyl-prolyl cis-trans isomerase (PPIase). PPIases accelerate the folding of proteins by catalyzing the cis-trans isomerization of proline imidic peptide bonds within oligopeptides.

Database Links

KEGG: ath:AT1G73655

STRING: 3702.AT1G73655.1

UniGene: At.17986

Protein Families

FKBP-type PPIase family

Subcellular Location

Plastid, chloroplast thylakoid lumen.

Q&A

Basic Research Questions

What is the role of FKBP3 in HIV-1 latency, and how can antibodies targeting it be experimentally validated?

FKBP3 promotes HIV-1 latency by recruiting histone deacetylases (HDAC1/2) to the viral long terminal repeat (LTR) via interaction with transcription factor YY1, leading to chromatin condensation .

Methodology:
- Use chromatin immunoprecipitation (ChIP) to confirm FKBP3 binding to the HIV-1 LTR .
- Perform co-immunoprecipitation (co-IP) assays to validate FKBP3-YY1-HDAC1/2 interactions in latent cell models (e.g., C11, J-Lat 10.6) .
- Measure latent HIV-1 reactivation via flow cytometry (GFP reporter) or qPCR for viral RNA after FKBP3 knockout .

What experimental models are suitable for studying FKBP3-mediated HIV-1 latency?

Model	Key Features	Utility
C11 cells	HIV-1 proviral DNA with GFP reporter; stable latency	Quantify reactivation via fluorescence
J-Lat 10.6	Clonal Jurkat cells with latent HIV-1	High-throughput drug screening
Primary CD4+ T cells	Patient-derived cells infected with HIV-1	Physiological relevance

How can researchers confirm FKBP3’s specificity in epigenetic regulation without off-target effects?

Approach:
- Use CRISPR/Cas9 with multiple sgRNAs to ensure consistent FKBP3 knockout phenotypes across cell lines .
- Perform RNA-seq to assess global gene expression changes post-knockout .
- Validate findings with rescue experiments (e.g., reintroduce wild-type FKBP3) .

Advanced Research Questions

What molecular mechanisms underlie FKBP3’s interaction with HDAC1/2 and YY1?

FKBP3 acts as a scaffold, bridging YY1 and HDAC1/2 to deacetylate histones at the HIV-1 LTR .

Key steps:
- Map binding domains via truncation mutants in co-IP assays.
- Use HDAC inhibitors (e.g., trichostatin A) to reverse FKBP3-mediated repression .
- Employ structural modeling (e.g., AlphaFold) to predict FKBP3-YY1 interface residues.

How does FKBP3 CRISPR screening improve latent HIV-1 activation strategies?

Parameter	FKBP3 Knockout	Control	Implications
HIV-1 reactivation	30–40% increase	Baseline	Validates FKBP3 as a latency regulator
Cell proliferation	Slight increase	No change	Low toxicity profile
Apoptosis	No change	No change	Safe for therapeutic targeting

Can FKBP3 targeting synergize with other latency-reversing agents (LRAs)?

Experimental design:
- Combine FKBP3 knockout with HDAC inhibitors (e.g., romidepsin) or PKC agonists (e.g., bryostatin-1).
- Measure synergistic effects using Bliss independence or Loewe additivity models .
- Assess viral rebound in primary cell models after sequential treatment .

What are the limitations of current FKBP3 studies in translational HIV cure research?

Critical gaps:
- Limited in vivo data: Most studies use cell lines (e.g., C11) or primary cells .
- Off-target risks: CRISPR may disrupt FKBP3’s native roles in protein folding .
- No small-molecule FKBP3 inhibitors reported; reliance on genetic knockout .

Methodological Considerations

Antibody validation: Use Western blotting with FKBP3-knockout lysates to confirm antibody specificity .
Data contradictions: Address variability in reactivation efficiency (e.g., 30% in C11 vs. 15% in ACH2 cells) by standardizing cell culture conditions .
Ethical constraints: Primary cell models require rigorous biosafety protocols for HIV-1 handling .

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FKBP17-3 Antibody