Anti-Prolactin Receptor Rabbit Monoclonal Antibody

Overview

This product is an anti-PRLR antibody for target detection and characterization. Key identifiers include host species: Rabbit; Monoclonal; clone ACIF-16; isotype Rabbit IgG; reactivity: Human,Mouse,Rat. Reported application contexts include WB, IHC, ICC, IF (as provided in the source record). Boster Bio Anti-Prolactin Receptor Rabbit Monoclonal Antibody catalog # M01196-2. Tested in WB, IHC, ICC/IF applications. This antibody reacts with Human, Mouse, Rat.

Key elements and design rationale

• Target: PRLR (HLA class II histocompatibility antigen, DR alpha chain).
• Antibody format: Monoclonal; clone ACIF-16; isotype Rabbit IgG.
• Host: Rabbit.
• Species reactivity: Human,Mouse,Rat (confirm in your model system with appropriate controls).

This description is intended to help interpret the antibody design and the biological context of the target using the fields provided in the catalog record, alongside general experimental considerations.

Biological background

PRLR (protein: Glycogen synthase kinase-3 beta (gsk3b)) is a commonly studied target in molecular and cellular biology. Functional context (as provided): Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal microenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading. Reported cellular localization context: Cell membrane; Single-pass type I membrane protein. Endoplasmic reticulum membrane; Single-pass type I membrane protein. Golgi apparatus, trans-Golgi network membrane; Single-pass type I membrane protein. Endosome membrane; Single- pass type I membrane protein. Lysosome membrane; Single-pass type I membrane protein. Late endosome membrane; Single-pass type I membrane protein. The MHC class II complex transits through a number of intracellular compartments in the endocytic pathway until it reaches the cell membrane for antigen presentation. Tissue expression notes (as provided): Ubiquitous. Expression is strongest in fetal and adult brain, spinal cord, and cerebellum, followed by thymus, bone marrow, testis, and fetal liver. Expression is intermediate in colon, ovary, placenta, uterus, and trachea, and is readily detected at substantially lower levels in all other tissues examined. Lowest expression is found in adult liver. Present in much greater abundance in cells from patients with acute leukemia of different subtypes than in normal peripheral blood lymphocytes, non-leukemic proliferating lymphoid cells, bone marrow cells, or cells from patients with chronic lymphoid or myeloid leukemia. .

Research relevance and current trends

• Research context keywords from the source record include: Cell Biology,Cell Cycle,Cell Differentiation,Growth Factors/Hormones,Signal Transduction.
• Current studies often focus on connecting target abundance/localization to pathway perturbations across models, tissues, and cell states.
• Quantitative and multiplexed assays (e.g., imaging + immunoblot panels) are commonly used to compare phenotypes across conditions and time-courses.

Common research applications

• Western blotting (WB): assess relative target abundance across samples, treatments, or time-points.
• Immunohistochemistry (IHC): evaluate spatial distribution of target-positive staining in tissue architecture.
• Immunofluorescence/ICC (IF/ICC): visualize subcellular localization patterns and cell-to-cell heterogeneity.

Workflow ideas (metafield): Validate PRLR antibody specificity using KO/KD control samples (WB/IF/IHC as appropriate), Detect PRLR expression by Western blot in cell or tissue lysates, Detect PRLR in FFPE tissue sections by immunohistochemistry, Localize PRLR by immunofluorescence/immunocytochemistry in cultured cells

Notes for experimental interpretation

• Consider isoforms and post-translational modifications (PTMs) that may shift apparent molecular weight or epitope accessibility.
• Apparent molecular weight may vary by sample type and processing (observed MW: 17 kDa; calculated MW: 28607 MW).
• Control concepts: include appropriate negative controls (e.g., isotype, KO/KD samples) and orthogonal validation when feasible.

Additional product details (from the source record)

• Molecular weight (observed): 17 kDa
• Cellular localization (provided): Cell membrane; Single-pass type I membrane protein. Endoplasmic reticulum membrane; Single-pass type I membrane protein. Golgi apparatus, trans-Golgi network membrane; Single-pass type I membrane protein. Endosome membrane; Single- pass type I membrane protein. Lysosome membrane; Single-pass type I membrane protein. Late endosome membrane; Single-pass type I membrane protein. The MHC class II complex transits through a number of intracellular compartments in the endocytic pathway until it reaches the cell membrane for antigen presentation.
• Tissue details (provided): Ubiquitous. Expression is strongest in fetal and adult brain, spinal cord, and cerebellum, followed by thymus, bone marrow, testis, and fetal liver. Expression is intermediate in colon, ovary, placenta, uterus, and trachea, and is readily detected at substantially lower levels in all other tissues examined. Lowest expression is found in adult liver. Present in much greater abundance in cells from patients with acute leukemia of different subtypes than in normal peripheral blood lymphocytes, non-leukemic proliferating lymphoid cells, bone marrow cells, or cells from patients with chronic lymphoid or myeloid leukemia. .

Customization & Add-ons: Can’t find the antibody you need—or require a custom format for your assay? We can help you source the best match or support custom antibody solutions for diverse research needs, including species and isotype selection, conjugations and labeling (e.g., HRP/AP, biotin, fluorophores), purification grade options (Protein A/G, affinity purified), formulation preferences (buffer selection, carrier-free, glycerol-free), custom concentrations and aliquoting, low-endotoxin options for cell-based work, and application-focused QC/validation support (project dependent). Click Talk to a Scientist to submit a request, email us at support@biohippo.com, or explore our Research Services for additional support—our team will follow up with feasibility details and next steps.