Customize FKBP16-3 Antibody

Description

Definition and Biological Role

FKBP16-3 Antibody is a polyclonal antibody primarily designed to detect FKBP16-3, a chloroplast-localized immunophilin with peptidyl-prolyl cis-trans isomerase (PPIase) activity. This protein plays critical roles in plant stress responses, including salinity, drought, and oxidative stress tolerance .

Stress Response Regulation

Expression Patterns:
- FKBP16-3 is predominantly expressed in photosynthetic tissues (e.g., leaves) and upregulated under abiotic stresses (salt, drought, H₂O₂, high light) .
- Transgenic Arabidopsis and rice overexpressing OsFKBP16-3 showed enhanced tolerance to salinity (150 mM NaCl) and oxidative stress (methyl viologen) .

Subcellular Localization

OsFKBP16-3-GFP fusion experiments confirmed chloroplast localization in Nicotiana benthamiana leaves .

Redox Sensitivity

Recombinant OsFKBP16-3 exists in oxidized (disulfide-bonded) and reduced forms, regulated by the CxxxC motif. Mutation of cysteines (C128,131S) abolished redox sensitivity .

Applications in Research

FKBP16-3 antibodies enable:

Protein Detection: Western blotting to validate FKBP16-3 expression in transgenic plants .
Stress Mechanism Studies: Investigating FKBP16-3’s role in maintaining photosynthetic apparatus integrity under stress .
Localization Analysis: Confirming chloroplast-specific expression via GFP tagging .

Table 1: Key Findings from OsFKBP16-3 Transgenic Studies

Parameter	Result
Salt Tolerance	80% survival in 150 mM NaCl (vs. 30% in controls)
Drought Resistance	2.5-fold higher relative water content in transgenic plants
Oxidative Stress	Reduced lipid peroxidation under methyl viologen treatment
Protein Expression	Confirmed via Western blot using species-specific antibodies

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

FKBP16-3 antibody; FKBP17 antibody; At2g43560 antibody; T1O24.30Peptidyl-prolyl cis-trans isomerase FKBP16-3 antibody; chloroplastic antibody; PPIase FKBP16-3 antibody; EC 5.2.1.8 antibody; FK506-binding protein 16-3 antibody; AtFKBP16-3 antibody; Immunophilin FKBP16-3 antibody; Rotamase antibody

Target Names

FKBP16-3

Uniprot No.

O22870

Target Background

Function

FKBP16-3 Antibody targets proteins called peptidyl-prolyl cis-trans isomerases (PPIases). These enzymes play a crucial role in protein folding by catalyzing the conversion of proline imidic peptide bonds from a cis to a trans configuration. This isomerization step is essential for the proper folding and function of many proteins.

Database Links

KEGG: ath:AT2G43560

STRING: 3702.AT2G43560.1

UniGene: At.24392

Protein Families

FKBP-type PPIase family

Subcellular Location

Plastid, chloroplast thylakoid lumen.

Q&A

FAQs for FKBP3 Antibody Research (Note: FKBP16-3 not directly referenced in literature; analysis focuses on FKBP3/FKBP11 family members)

Advanced Research Questions

How to resolve contradictions in FKBP3’s role during acute vs. latent HIV-1 infection?
Data Analysis Framework:

Infection Phase	FKBP3 Activity	Experimental Evidence
Acute infection	Inhibits HIV replication	Overexpression in TZM-bl cells reduces luciferase activity (Fig. 5B in )
Latent infection	Sustains viral dormancy	KO increases GFP+ cells by 30% in C11 model (Fig. 1A in )

Resolution Strategy:

Use time-course RNA-seq to track FKBP3 expression dynamics post-infection.
Validate context-dependent interactions (e.g., stress granules in acute infection vs. chromatin remodeling in latency) .

What are the limitations of current FKBP3-targeting strategies for HIV cure research?
Critical Challenges:
- Off-target effects: RNAi/CRISPR may perturb unrelated immunophilin pathways (e.g., FKBP11 in antibody folding ).
- Partial latency reversal: FKBP3 KO reactivates only 30% of latent HIV (Fig. 1A in ), necessitating combinatorial approaches (e.g., HDAC inhibitors).
- Safety: While FKBP3 KO does not induce apoptosis (Fig. S3 in ), long-term immune impacts remain unstudied.

Methodological Guidance

How to design a CRISPR screen for identifying FKBP3-associated latency factors?
Stepwise Protocol:
1. Library design: Use a pooled sgRNA library targeting immunophilins and epigenetic regulators.
2. Screening: Infect Jurkat T-cells with HIV-1-NanoLuc, apply latency-reversing agents (LRAs), and sort cells based on luciferase activity .
3. Hit validation: Prioritize genes with ≥2-fold change in sgRNA abundance (e.g., FKBP3 in ).
4. Mechanistic follow-up: Combine ChIP, Co-IP, and RNA-seq to map pathways.
How to assess FKBP3’s role in antibody folding (e.g., in plasma cells)?
Experimental Workflow:
- Model system: Differentiate human B-cells into plasma cells using IL-6/IL-21 .
- Knockdown/overexpression: Use lentiviral shRNA or FKBP11 (homolog)-tagged constructs (e.g., pCAG vectors ).
- Readouts: Measure IgM/IgG secretion (ELISA), ER stress markers (XBP1 splicing), and FKBP3-FKBP11 colocalization (immunofluorescence) .

Data Interpretation Tables

Table 1: FKBP3 Knockout Efficacy in Latent HIV Models

Cell Line	FKBP3 KO Reactivation (%)	Key Assay
C11	30 ± 5	Flow cytometry (GFP)
J-Lat 10.6	25 ± 4	Luciferase assay
Primary CD4+	22 ± 3	NanoLuc/p24 ELISA

Table 2: FKBP3 Interaction Partners in HIV Latency

Protein	Interaction Confirmed?	Method	Functional Role
YY1	Yes (Co-IP)	Co-IP/Western blot	Recruits HDAC1/2 to LTR
HDAC1	Yes	Co-IP/ChIP-qPCR	Deacetylates histones H3/H4
HDAC2	Yes	Co-IP/ChIP-qPCR	Synergizes with HDAC1

Key Research Gaps

Structural basis of FKBP3-LTR binding (cryo-EM data lacking).
Tissue-specific FKBP3 isoforms and their roles in non-HIV pathologies (e.g., IPF ).
Cross-reactivity of anti-FKBP3 antibodies with FKBP11 or other immunophilins .

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FKBP16-3 Antibody