Klotho, also called Klotho-alpha, is the founding member of the Klotho family within the glycosidase-1 superfamily (1, 2). Klotho is expressed in areas concerned with calcium regulation, predominantly in the kidney distal convoluted tubules, but also in the brain choroid plexus (which produces cerebrospinal fluid) and the parathyroid (1). The 1014 amino acid (aa) type I transmembrane protein contains a 34 aa signal sequence, a 948 aa extracellular domain (ECD) containing two extracellular glycosidase-like domains, a 21 aa transmembrane domain and an 11 aa intracellular domain. Within the ECD, mouse Klotho shares 95%, 87%, and 87% aa identity with rat, human, and equine Klotho, respectively. Although a truncated 554 aa isoform predicts a soluble 70 kDa form, the soluble form found in plasma and cerebrospinal fluid is a 130 kDa form produced by proteolytic cleavage of the glycosylated 135 kDa full-length Klotho (3, 4). A prominent intracellular 120 kDa form of Klotho is localized to endoplasmic reticulum and Golgi membranes (4). Klotho is named for the Greek goddess who spins the thread of life. The phenotype of Klotho-deficient mice resembles premature aging, including arteriosclerosis, osteoporosis, skin atrophy, infertility, emphysema, and premature death (2). Conversely, excess Klotho extends lifespan (5). Klotho acts as a cofactor for interaction of FGF-23 with FGF R1 (6). This interaction negatively regulates 1 alpha -hydroxylase, the rate-limiting enzyme in the synthesis of 1,25(OH)2D3 (vitamin D) (7). Klotho-deficient mice show severe hyperphosphatemia and ectopic calcification of soft tissues due to excess vitamin D (2, 7). Both Klotho and Klotho-beta are co-factors for FGF-19 binding (8). Klotho also shows glucuronidase activity which activates the renal ion channel TRPV5 to reabsorb urinary calcium (9). Klotho has been reported to downregulate insulin or IGF-I signaling in adipocytes, to bind and antagonize Wnt molecules, and to facilitate release of parathyroid hormone (10-12).
Key Product Details
Species Reactivity
Validated:
Mouse
Cited:
Human, Mouse, Nematode - Caenorhabditis elegans
Applications
Validated:
Immunohistochemistry, ELISA
Cited:
Immunohistochemistry, Western Blot, Immunoprecipitation
Label
Unconjugated
Antibody Source
Monoclonal Rat IgG2A Clone # 236214
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Product Specifications
Immunogen
Mouse myeloma cell line NS0-derived recombinant mouse Klotho
Specificity
Detects mouse Klotho (aa 23-550 and aa 35-982) in direct ELISAs and Western blots. Does not cross-react with recombinant human Klotho or recombinant mouse Klotho B.
Clonality
Monoclonal
Host
Rat
Isotype
IgG2A
Scientific Data Images for Mouse Klotho Antibody
Mouse Klotho ELISA Standard Curve.
Recombinant Mouse Klotho protein was serially diluted 2-fold and captured by Rat Anti-Mouse Klotho Monoclonal Antibody (Catalog # MAB1819) coated on a Clear Polystyrene Microplate (Catalog # DY990). Goat Anti-Mouse Klotho Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1819) was biotinylated and incubated with the protein captured on the plate. Detection of the standard curve was achieved by incubating Streptavidin-HRP (Catalog # DY998) followed by Substrate Solution (Catalog # DY999) and stopping the enzymatic reaction with Stop Solution (Catalog # DY994).
Detection of Mouse Klotho by Immunocytochemistry/ Immunofluorescence
Epigenetic regulation of alpha -Klotho by stiff matrix disrupts chondrocytes health. A Stiff substrates downregulated Klotho expression and increased Klotho promoter methylation as well as global DNA methylation in young chondrocytes (n = 3/group). B Stiff substrates increased DNMT1 expression in young chondrocytes as quantified by immunofluorescence (n = 5/group; 30–50 cells per individual sample). Scale bar: 20 μm. C Stiff substrates increased binding of DNMT1 at Klotho promoter in young chondrocytes quantified by chromatin immunoprecipitation (ChIP) analyses (n = 4/group). D Stiff substrates increased binding of RNA Polymerase II (Pol II), active chromatin mark H3K4M2, and c-MYC, but not the repressive chromatin mark, H3K9M2, at the Dnmt1 promoter in young chondrocytes, as quantified by ChIP analyses (n = 4/group). E, F siRNA Dnmt1 treatment inhibited the deleterious effect of a stiff microenvironment on alpha -Klotho, type II collagen (Col2), and aggrecan (Acan) expression, as quantified by immunofluorescence (n = 4/group; 40–50 cells per individual sample). Scale bar: 50 μm. G, H 5-Aza-2’-deoxycytidine (5 Aza) treatment inhibits the deleterious effect of a stiff microenvironment on alpha -Klotho, Col2, and Acan expression. The effects of 5 Aza treatment were blocked when combined with siRNA Klotho (siRNA KL) treatment. Data were quantified by immunofluorescence (n = 4/group; 30–45 cells per individual sample). Scale bar: 50 μm. Statistical analyses were performed using a linear mixed effect model (A–D), two-tailed paired t test (E–G) or analysis of variance with post-hoc Tukey–Kramer test (H). **p < 0.01, ***p < 0.001. Data are presented as means ±95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of Mouse Klotho by Immunocytochemistry/ Immunofluorescence
Epigenetic regulation of alpha -Klotho by stiff matrix disrupts chondrocytes health. A Stiff substrates downregulated Klotho expression and increased Klotho promoter methylation as well as global DNA methylation in young chondrocytes (n = 3/group). B Stiff substrates increased DNMT1 expression in young chondrocytes as quantified by immunofluorescence (n = 5/group; 30–50 cells per individual sample). Scale bar: 20 μm. C Stiff substrates increased binding of DNMT1 at Klotho promoter in young chondrocytes quantified by chromatin immunoprecipitation (ChIP) analyses (n = 4/group). D Stiff substrates increased binding of RNA Polymerase II (Pol II), active chromatin mark H3K4M2, and c-MYC, but not the repressive chromatin mark, H3K9M2, at the Dnmt1 promoter in young chondrocytes, as quantified by ChIP analyses (n = 4/group). E, F siRNA Dnmt1 treatment inhibited the deleterious effect of a stiff microenvironment on alpha -Klotho, type II collagen (Col2), and aggrecan (Acan) expression, as quantified by immunofluorescence (n = 4/group; 40–50 cells per individual sample). Scale bar: 50 μm. G, H 5-Aza-2’-deoxycytidine (5 Aza) treatment inhibits the deleterious effect of a stiff microenvironment on alpha -Klotho, Col2, and Acan expression. The effects of 5 Aza treatment were blocked when combined with siRNA Klotho (siRNA KL) treatment. Data were quantified by immunofluorescence (n = 4/group; 30–45 cells per individual sample). Scale bar: 50 μm. Statistical analyses were performed using a linear mixed effect model (A–D), two-tailed paired t test (E–G) or analysis of variance with post-hoc Tukey–Kramer test (H). **p < 0.01, ***p < 0.001. Data are presented as means ±95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of Mouse Klotho by Immunocytochemistry/ Immunofluorescence
Epigenetic regulation of alpha -Klotho by stiff matrix disrupts chondrocytes health. A Stiff substrates downregulated Klotho expression and increased Klotho promoter methylation as well as global DNA methylation in young chondrocytes (n = 3/group). B Stiff substrates increased DNMT1 expression in young chondrocytes as quantified by immunofluorescence (n = 5/group; 30–50 cells per individual sample). Scale bar: 20 μm. C Stiff substrates increased binding of DNMT1 at Klotho promoter in young chondrocytes quantified by chromatin immunoprecipitation (ChIP) analyses (n = 4/group). D Stiff substrates increased binding of RNA Polymerase II (Pol II), active chromatin mark H3K4M2, and c-MYC, but not the repressive chromatin mark, H3K9M2, at the Dnmt1 promoter in young chondrocytes, as quantified by ChIP analyses (n = 4/group). E, F siRNA Dnmt1 treatment inhibited the deleterious effect of a stiff microenvironment on alpha -Klotho, type II collagen (Col2), and aggrecan (Acan) expression, as quantified by immunofluorescence (n = 4/group; 40–50 cells per individual sample). Scale bar: 50 μm. G, H 5-Aza-2’-deoxycytidine (5 Aza) treatment inhibits the deleterious effect of a stiff microenvironment on alpha -Klotho, Col2, and Acan expression. The effects of 5 Aza treatment were blocked when combined with siRNA Klotho (siRNA KL) treatment. Data were quantified by immunofluorescence (n = 4/group; 30–45 cells per individual sample). Scale bar: 50 μm. Statistical analyses were performed using a linear mixed effect model (A–D), two-tailed paired t test (E–G) or analysis of variance with post-hoc Tukey–Kramer test (H). **p < 0.01, ***p < 0.001. Data are presented as means ±95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of Mouse Klotho by Immunocytochemistry/ Immunofluorescence
Age-related declines in alpha -Klotho are associated with cartilage degeneration in male mice. A Aging induced a progressive decline of alpha -Klotho in the murine medial tibia (n = 5/sex/age). White arrows indicate alpha -Klotho-positive chondrocytes. White dashed lines indicate cartilage surface. AC articular cartilage. Scale bar: 10 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (50–100 cells per mouse). B Cartilage in older adults (≥65 years old; 71.9 ± 2.91 years; n = 7 [1 female]) displayed reduced alpha -Klotho expression compared to young adults (<40 years old; 27.6 ± 6.85 years; n = 7 [2 females]). Scale bar: 20 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (30–70 cells per cartilage sample). C Loss-of function in Klotho (Klotho+/−) triggered murine cartilage degeneration in a sex-dependent manner (young, n = 7 for wild-type [3 females], n = 10 for Klotho+/− [5 females]; middle-aged, n = 10 for wild-type [5 females], n = 8 for Klotho+/− [5 females]). Black arrows indicate cartilage surface disruption. AC articular cartilage. Scale bar: 50 μm. Statistical analyses were performed using linear regression (A), two-way ANOVA (C), and a two-tailed Student t test (B). Age-sex interaction was not significant for alpha -Klotho expression in mice (A, p = 0.468). Data are presented as means ± 95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of Mouse Klotho by Immunocytochemistry/ Immunofluorescence
Age-related declines in alpha -Klotho are associated with cartilage degeneration in male mice. A Aging induced a progressive decline of alpha -Klotho in the murine medial tibia (n = 5/sex/age). White arrows indicate alpha -Klotho-positive chondrocytes. White dashed lines indicate cartilage surface. AC articular cartilage. Scale bar: 10 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (50–100 cells per mouse). B Cartilage in older adults (≥65 years old; 71.9 ± 2.91 years; n = 7 [1 female]) displayed reduced alpha -Klotho expression compared to young adults (<40 years old; 27.6 ± 6.85 years; n = 7 [2 females]). Scale bar: 20 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (30–70 cells per cartilage sample). C Loss-of function in Klotho (Klotho+/−) triggered murine cartilage degeneration in a sex-dependent manner (young, n = 7 for wild-type [3 females], n = 10 for Klotho+/− [5 females]; middle-aged, n = 10 for wild-type [5 females], n = 8 for Klotho+/− [5 females]). Black arrows indicate cartilage surface disruption. AC articular cartilage. Scale bar: 50 μm. Statistical analyses were performed using linear regression (A), two-way ANOVA (C), and a two-tailed Student t test (B). Age-sex interaction was not significant for alpha -Klotho expression in mice (A, p = 0.468). Data are presented as means ± 95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of Klotho by Immunocytochemistry/ Immunofluorescence
Age-related declines in alpha -Klotho are associated with cartilage degeneration in male mice. A Aging induced a progressive decline of alpha -Klotho in the murine medial tibia (n = 5/sex/age). White arrows indicate alpha -Klotho-positive chondrocytes. White dashed lines indicate cartilage surface. AC articular cartilage. Scale bar: 10 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (50–100 cells per mouse). B Cartilage in older adults (≥65 years old; 71.9 ± 2.91 years; n = 7 [1 female]) displayed reduced alpha -Klotho expression compared to young adults (<40 years old; 27.6 ± 6.85 years; n = 7 [2 females]). Scale bar: 20 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (30–70 cells per cartilage sample). C Loss-of function in Klotho (Klotho+/−) triggered murine cartilage degeneration in a sex-dependent manner (young, n = 7 for wild-type [3 females], n = 10 for Klotho+/− [5 females]; middle-aged, n = 10 for wild-type [5 females], n = 8 for Klotho+/− [5 females]). Black arrows indicate cartilage surface disruption. AC articular cartilage. Scale bar: 50 μm. Statistical analyses were performed using linear regression (A), two-way ANOVA (C), and a two-tailed Student t test (B). Age-sex interaction was not significant for alpha -Klotho expression in mice (A, p = 0.468). Data are presented as means ± 95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of Mouse Klotho by Immunocytochemistry/ Immunofluorescence
Epigenetic regulation of alpha -Klotho by stiff matrix disrupts chondrocytes health. A Stiff substrates downregulated Klotho expression and increased Klotho promoter methylation as well as global DNA methylation in young chondrocytes (n = 3/group). B Stiff substrates increased DNMT1 expression in young chondrocytes as quantified by immunofluorescence (n = 5/group; 30–50 cells per individual sample). Scale bar: 20 μm. C Stiff substrates increased binding of DNMT1 at Klotho promoter in young chondrocytes quantified by chromatin immunoprecipitation (ChIP) analyses (n = 4/group). D Stiff substrates increased binding of RNA Polymerase II (Pol II), active chromatin mark H3K4M2, and c-MYC, but not the repressive chromatin mark, H3K9M2, at the Dnmt1 promoter in young chondrocytes, as quantified by ChIP analyses (n = 4/group). E, F siRNA Dnmt1 treatment inhibited the deleterious effect of a stiff microenvironment on alpha -Klotho, type II collagen (Col2), and aggrecan (Acan) expression, as quantified by immunofluorescence (n = 4/group; 40–50 cells per individual sample). Scale bar: 50 μm. G, H 5-Aza-2’-deoxycytidine (5 Aza) treatment inhibits the deleterious effect of a stiff microenvironment on alpha -Klotho, Col2, and Acan expression. The effects of 5 Aza treatment were blocked when combined with siRNA Klotho (siRNA KL) treatment. Data were quantified by immunofluorescence (n = 4/group; 30–45 cells per individual sample). Scale bar: 50 μm. Statistical analyses were performed using a linear mixed effect model (A–D), two-tailed paired t test (E–G) or analysis of variance with post-hoc Tukey–Kramer test (H). **p < 0.01, ***p < 0.001. Data are presented as means ±95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.
Detection of Klotho by Immunocytochemistry/ Immunofluorescence
Age-related declines in alpha -Klotho are associated with cartilage degeneration in male mice. A Aging induced a progressive decline of alpha -Klotho in the murine medial tibia (n = 5/sex/age). White arrows indicate alpha -Klotho-positive chondrocytes. White dashed lines indicate cartilage surface. AC articular cartilage. Scale bar: 10 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (50–100 cells per mouse). B Cartilage in older adults (≥65 years old; 71.9 ± 2.91 years; n = 7 [1 female]) displayed reduced alpha -Klotho expression compared to young adults (<40 years old; 27.6 ± 6.85 years; n = 7 [2 females]). Scale bar: 20 μm. alpha -Klotho expression per cell was quantified by immunofluorescence (30–70 cells per cartilage sample). C Loss-of function in Klotho (Klotho+/−) triggered murine cartilage degeneration in a sex-dependent manner (young, n = 7 for wild-type [3 females], n = 10 for Klotho+/− [5 females]; middle-aged, n = 10 for wild-type [5 females], n = 8 for Klotho+/− [5 females]). Black arrows indicate cartilage surface disruption. AC articular cartilage. Scale bar: 50 μm. Statistical analyses were performed using linear regression (A), two-way ANOVA (C), and a two-tailed Student t test (B). Age-sex interaction was not significant for alpha -Klotho expression in mice (A, p = 0.468). Data are presented as means ± 95% confidence intervals. Source data are provided as a Source Data file. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36627269), licensed under a CC-BY license. Not internally tested by R&D Systems.Applications for Mouse Klotho Antibody
Application
Recommended Usage
ELISA
This antibody functions as an ELISA capture antibody when paired with Goat Anti-Mouse Klotho Antigen Affinity-purified Polyclonal Antibody (Catalog # AF1819).
This product is intended for assay development on various assay platforms requiring antibody pairs.
Immunohistochemistry
8-25 µg/mL
Sample: Perfusion fixed frozen sections of mouse kindney and intestine.
Sample: Perfusion fixed frozen sections of mouse kindney and intestine.
Reviewed Applications
Read 1 review rated 5 using MAB1819 in the following applications:
Formulation, Preparation, and Storage
Purification
Protein A or G purified from hybridoma culture supernatant
Reconstitution
Reconstitute at 0.5 mg/mL in sterile PBS. For liquid material, refer to CoA for concentration.
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Formulation
Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.
Shipping
Lyophilized product is shipped at ambient temperature. Liquid small pack size (-SP) is shipped with polar packs. Upon receipt, store immediately at the temperature recommended below.
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Calculators
Background: Klotho
References
- Nabeshima, Y. (2006) Sci. Aging Knowl. Environ. 8:pe11.
- Kuro-o, M. et al. (1997) Nature 390:45.
- Shiraki-Iida, T. et al. (1998) FEBS Lett. 424:6.
- Imura, A. et al. (2004) FEBS Lett. 565:143.
- Kurosu, H. et al. (2005) Science 309:1829.
- Kurosu, H. et al. (2006) J. Biol. Chem. 281:6120.
- Tsujikawa, H. et al. (2003) Mol. Endocrinol. 17:2393.
- Wu, X. et al. (2007) J. Biol. Chem. 282:29069.
- Chang, Q. et al. (2005) Science 310:490.
- Yamamoto, M. et al. (2005) J. Biol. Chem. 280:38029.
- Liu, H. et al. (2007) Science 317:803.
- Imura, A. et al. (2007) Science 316:1615.
Alternate Names
KL
Gene Symbol
KL
Additional Klotho Products
Product Documents for Mouse Klotho Antibody
Certificate of Analysis
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Note: Certificate of Analysis not available for kit components.
Product Specific Notices for Mouse Klotho Antibody
For research use only
Related Research Areas
Citations for Mouse Klotho Antibody
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Application: ImmunoprecipitationSample Tested: C. elegans proteinsSpecies: elegansVerified Customer | Posted 03/18/2022
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Protocols
Find general support by application which include: protocols, troubleshooting, illustrated assays, videos and webinars.
- Antigen Retrieval Protocol (PIER)
- Antigen Retrieval for Frozen Sections Protocol
- Appropriate Fixation of IHC/ICC Samples
- Cellular Response to Hypoxia Protocols
- Chromogenic IHC Staining of Formalin-Fixed Paraffin-Embedded (FFPE) Tissue Protocol
- Chromogenic Immunohistochemistry Staining of Frozen Tissue
- ClariTSA™ Fluorophore Kits
- Detection & Visualization of Antibody Binding
- ELISA Sample Preparation & Collection Guide
- ELISA Troubleshooting Guide
- Fluorescent IHC Staining of Frozen Tissue Protocol
- Graphic Protocol for Heat-induced Epitope Retrieval
- Graphic Protocol for the Preparation and Fluorescent IHC Staining of Frozen Tissue Sections
- Graphic Protocol for the Preparation and Fluorescent IHC Staining of Paraffin-embedded Tissue Sections
- Graphic Protocol for the Preparation of Gelatin-coated Slides for Histological Tissue Sections
- How to Run an R&D Systems DuoSet ELISA
- How to Run an R&D Systems Quantikine ELISA
- How to Run an R&D Systems Quantikine™ QuicKit™ ELISA
- IHC Sample Preparation (Frozen sections vs Paraffin)
- Immunofluorescent IHC Staining of Formalin-Fixed Paraffin-Embedded (FFPE) Tissue Protocol
- Immunohistochemistry (IHC) and Immunocytochemistry (ICC) Protocols
- Immunohistochemistry Frozen Troubleshooting
- Immunohistochemistry Paraffin Troubleshooting
- Preparing Samples for IHC/ICC Experiments
- Preventing Non-Specific Staining (Non-Specific Binding)
- Primary Antibody Selection & Optimization
- Protocol for Heat-Induced Epitope Retrieval (HIER)
- Protocol for Making a 4% Formaldehyde Solution in PBS
- Protocol for VisUCyte™ HRP Polymer Detection Reagent
- Protocol for the Preparation & Fixation of Cells on Coverslips
- Protocol for the Preparation and Chromogenic IHC Staining of Frozen Tissue Sections
- Protocol for the Preparation and Chromogenic IHC Staining of Frozen Tissue Sections - Graphic
- Protocol for the Preparation and Chromogenic IHC Staining of Paraffin-embedded Tissue Sections
- Protocol for the Preparation and Chromogenic IHC Staining of Paraffin-embedded Tissue Sections - Graphic
- Protocol for the Preparation and Fluorescent IHC Staining of Frozen Tissue Sections
- Protocol for the Preparation and Fluorescent IHC Staining of Paraffin-embedded Tissue Sections
- Protocol for the Preparation of Gelatin-coated Slides for Histological Tissue Sections
- Quantikine HS ELISA Kit Assay Principle, Alkaline Phosphatase
- Quantikine HS ELISA Kit Principle, Streptavidin-HRP Polymer
- Sandwich ELISA (Colorimetric) – Biotin/Streptavidin Detection Protocol
- Sandwich ELISA (Colorimetric) – Direct Detection Protocol
- TUNEL and Active Caspase-3 Detection by IHC/ICC Protocol
- The Importance of IHC/ICC Controls
- Troubleshooting Guide: ELISA
- Troubleshooting Guide: Immunohistochemistry
- View all Protocols, Troubleshooting, Illustrated assays and Webinars
FAQs for Mouse Klotho Antibody
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Q: Does Mouse Klotho antibody, Catalog # MAB1819, cross react with Rat?
A: When Rat Samples were tested with this antibody, we did observe a positive result in Western Blot. We would expect this antibody to recognize Rat samples, but have not done extensive validation testing for samples from this species.
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