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Tags & Cell Markers Subcellular Markers Nucleus Nuclear Envelope
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Validated using a knockout cell line

HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636)

  • Datasheet
  • SDS
Submit a review Q&A (1)References (11)

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Western blot - HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636)
  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636)

Key features and details

  • HRP Mouse monoclonal [JOL2] to Lamin A + Lamin C
  • Suitable for: IHC-P, WB
  • Knockout validated
  • Reacts with: Human, African green monkey
  • Conjugation: HRP
  • Isotype: IgG1

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Overview

  • Product name

    HRP Anti-Lamin A + Lamin C antibody [JOL2]
    See all Lamin A + Lamin C primary antibodies
  • Description

    HRP Mouse monoclonal [JOL2] to Lamin A + Lamin C
  • Host species

    Mouse
  • Conjugation

    HRP
  • Tested applications

    Suitable for: IHC-P, WBmore details
  • Species reactivity

    Reacts with: Human, African green monkey
  • Immunogen

    Recombinant fragment corresponding to Human Lamin A + Lamin C.

  • Epitope

    This product has been shown to bind to an epitope between amino acids 464-572.
  • Positive control

    • WB: HAP1, HeLa and HepG2 cell lysate IHC-P: Human young placenta, tonsil.
  • General notes

    Reproducibility is key to advancing scientific discovery and accelerating scientists’ next breakthrough.

    Abcam is leading the way with our range of recombinant antibodies, knockout-validated antibodies and knockout cell lines, all of which support improved reproducibility.

    We are also planning to innovate the way in which we present recommended applications and species on our product datasheets, so that only applications & species that have been tested in our own labs, our suppliers or by selected trusted collaborators are covered by our Abpromise™ guarantee.

    In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.

    We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.

    Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.

    Please check that this product meets your needs before purchasing. If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, as well as customer reviews and Q&As.

Properties

  • Form

    Liquid
  • Storage instructions

    Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term.
  • Storage buffer

    pH: 7.40
    Preservative: 0.01% Thimerosal (merthiolate)
    Constituent: PBS
  • Concentration information loading...
  • Purity

    Protein G purified
  • Clonality

    Monoclonal
  • Clone number

    JOL2
  • Myeloma

    Sp2/0-Ag14
  • Isotype

    IgG1
  • Research areas

    • Tags & Cell Markers
    • Subcellular Markers
    • Nucleus
    • Nuclear Envelope
    • Signal Transduction
    • Cytoskeleton / ECM
    • Cytoskeleton
    • Intermediate Filaments
    • Class V
    • Lamins

Associated products

  • Alternative Versions

    • Anti-Lamin A + Lamin C antibody [JOL2] (ab40567)
  • Isotype control

    • Mouse IgG1, Kappa Monoclonal [B11/6] - Isotype Control (ab91353)

Applications

Our Abpromise guarantee covers the use of ab196636 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P Use a concentration of 4 µg/ml.
WB 1/200. Predicted molecular weight: 74 kDa.

Target

  • Function

    Lamins are components of the nuclear lamina, a fibrous layer on the nucleoplasmic side of the inner nuclear membrane, which is thought to provide a framework for the nuclear envelope and may also interact with chromatin. Lamin A and C are present in equal amounts in the lamina of mammals. Play an important role in nuclear assembly, chromatin organization, nuclear membrane and telomere dynamics.
    Prelamin-A/C can accelerate smooth muscle cell senescence. It acts to disrupt mitosis and induce DNA damage in vascular smooth muscle cells (VSMCs), leading to mitotic failure, genomic instability, and premature senescence.
  • Tissue specificity

    In the arteries, prelamin-A/C accumulation is not observed in young healthy vessels but is prevalent in medial vascular smooth muscle celle (VSMCs) from aged individuals and in atherosclerotic lesions, where it often colocalizes with senescent and degenerate VSMCs. Prelamin-A/C expression increases with age and disease. In normal aging, the accumulation of prelamin-A/C is caused in part by the down-regulation of ZMPSTE24/FACE1 in response to oxidative stress.
  • Involvement in disease

    Defects in LMNA are the cause of Emery-Dreifuss muscular dystrophy type 2 (EDMD2) [MIM:181350]. A degenerative myopathy characterized by weakness and atrophy of muscle without involvement of the nervous system, early contractures of the elbows, Achilles tendons and spine, and cardiomyopathy associated with cardiac conduction defects.
    Defects in LMNA are the cause of cardiomyopathy dilated type 1A (CMD1A) [MIM:115200]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
    Defects in LMNA are the cause of familial partial lipodystrophy type 2 (FPLD2) [MIM:151660]; also known as familial partial lipodystrophy Dunnigan type. A disorder characterized by the loss of subcutaneous adipose tissue in the lower parts of the body (limbs, buttocks, trunk). It is accompanied by an accumulation of adipose tissue in the face and neck causing a double chin, fat neck, or cushingoid appearance. Adipose tissue may also accumulate in the axillae, back, labia majora, and intraabdominal region. Affected patients are insulin-resistant and may develop glucose intolerance and diabetes mellitus after age 20 years, hypertriglyceridemia, and low levels of high density lipoprotein cholesterol.
    Defects in LMNA are the cause of limb-girdle muscular dystrophy type 1B (LGMD1B) [MIM:159001]. LGMD1B is an autosomal dominant degenerative myopathy with age-related atrioventricular cardiac conduction disturbances, dilated cardiomyopathy, and the absence of early contractures. LGMD1B is characterized by slowly progressive skeletal muscle weakness of the hip and shoulder girdles. Muscle biopsy shows mild dystrophic changes.
    Defects in LMNA are the cause of Charcot-Marie-Tooth disease type 2B1 (CMT2B1) [MIM:605588]. CMT2B1 is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy. CMT2B1 inheritance is autosomal recessive.
    Defects in LMNA are the cause of Hutchinson-Gilford progeria syndrome (HGPS) [MIM:176670]. HGPS is a rare genetic disorder characterized by features reminiscent of marked premature aging. Note=HGPS is caused by the toxic accumulation of a mutant form of lamin-A/C. This mutant protein, called progerin, acts to deregulate mitosis and DNA damage signaling, leading to premature cell death and senescence. Progerin lacks the conserved ZMPSTE24/FACE1 cleavage site and therefore remains permanently farnesylated. Thus, although it can enter the nucleus and associate with the nuclear envelope, it cannot incorporate normally into the nuclear lamina.
    Defects in LMNA are the cause of cardiomyopathy dilated with hypergonadotropic hypogonadism (CMDHH) [MIM:212112]. A disorder characterized by the association of genital anomalies, hypergonadotropic hypogonadism and dilated cardiomyopathy. Patients can present other variable clinical manifestations including mental retardation, skeletal anomalies, scleroderma-like skin, graying and thinning of hair, osteoporosis. Dilated cardiomyopathy is characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia.
    Defects in LMNA are the cause of mandibuloacral dysplasia with type A lipodystrophy (MADA) [MIM:248370]. A disorder characterized by mandibular and clavicular hypoplasia, acroosteolysis, delayed closure of the cranial suture, progeroide appearance, partial alopecia, soft tissue calcinosis, joint contractures, and partial lipodystrophy with loss of subcutaneous fat from the extremities. Adipose tissue in the face, neck and trunk is normal or increased.
    Defects in LMNA are a cause of lethal tight skin contracture syndrome (LTSCS) [MIM:275210]; also known as restrictive dermopathy (RD). Lethal tight skin contracture syndrome is a rare disorder mainly characterized by intrauterine growth retardation, tight and rigid skin with erosions, prominent superficial vasculature and epidermal hyperkeratosis, facial features (small mouth, small pinched nose and micrognathia), sparse/absent eyelashes and eyebrows, mineralization defects of the skull, thin dysplastic clavicles, pulmonary hypoplasia, multiple joint contractures and an early neonatal lethal course. Liveborn children usually die within the first week of life. The overall prevalence of consanguineous cases suggested an autosomal recessive inheritance.
    Defects in LMNA are the cause of heart-hand syndrome Slovenian type (HHS-Slovenian) [MIM:610140]. Heart-hand syndrome (HHS) is a clinically and genetically heterogeneous disorder characterized by the co-occurrence of a congenital cardiac disease and limb malformations.
    Defects in LMNA are the cause of muscular dystrophy congenital LMNA-related (CMD-LMNA) [MIM:613205]. It is a form of congenital muscular dystrophy. Patients present at birth, or within the first few months of life, with hypotonia, muscle weakness and often with joint contractures.
  • Sequence similarities

    Belongs to the intermediate filament family.
  • Post-translational
    modifications

    Increased phosphorylation of the lamins occurs before envelope disintegration and probably plays a role in regulating lamin associations.
    Proteolytic cleavage of the C-terminal of 18 residues of prelamin-A/C results in the production of lamin-A/C. The prelamin-A/C maturation pathway includes farnesylation of CAAX motif, ZMPSTE24/FACE1 mediated cleavage of the last three amino acids, methylation of the C-terminal cysteine and endoproteolytic removal of the last 15 C-terminal amino acids. Proteolytic cleavage requires prior farnesylation and methylation, and absence of these blocks cleavage.
    Sumoylation is necessary for the localization to the nuclear envelope.
    Farnesylation of prelamin-A/C facilitates nuclear envelope targeting.
  • Cellular localization

    Nucleus. Nucleus envelope. Farnesylation of prelamin-A/C facilitates nuclear envelope targeting and subsequent cleaveage by ZMPSTE24/FACE1 to remove the farnesyl group produces mature lamin-A/C, which can then be inserted into the nuclear lamina. EMD is required for proper localization of non-farnesylated prelamin-A/C.
  • Target information above from: UniProt accession P02545 The UniProt Consortium
    The Universal Protein Resource (UniProt) in 2010
    Nucleic Acids Res. 38:D142-D148 (2010) .

    Information by UniProt
  • Database links

    • Entrez Gene: 103223838 African green monkey
    • Entrez Gene: 4000 Human
    • Omim: 150330 Human
    • SwissProt: P02545 Human
    • Unigene: 594444 Human
    • Alternative names

      • 70 kDa lamin antibody
      • Cardiomyopathy dilated 1A (autosomal dominant) antibody
      • CDCD1 antibody
      • CDDC antibody
      • CMD1A antibody
      • CMT2B1 antibody
      • EMD2 antibody
      • FPL antibody
      • FPLD antibody
      • FPLD2 antibody
      • HGPS antibody
      • IDC antibody
      • Lamin A antibody
      • Lamin A/C antibody
      • Lamin A/C like 1 antibody
      • Lamin antibody
      • Lamin C antibody
      • lamin-a antibody
      • Lamin-A/C antibody
      • LDP1 antibody
      • LFP antibody
      • LGMD1B antibody
      • Limb girdle muscular dystrophy 1B (autosomal dominant) antibody
      • LMN 1 antibody
      • LMN A antibody
      • LMN C antibody
      • LMN1 antibody
      • LMNA antibody
      • LMNA_HUMAN antibody
      • LMNC antibody
      • LMNL1 antibody
      • Prelamin A/C antibody
      • PRO1 antibody
      • Renal carcinoma antigen NY REN 32 antibody
      • Renal carcinoma antigen NY-REN-32 antibody
      • Renal carcinoma antigen NYREN32 antibody
      see all

    Images

    • Western blot - HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636)
      Western blot - HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636)
      All lanes : HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636) at 1/200 dilution

      Lane 1 : Wild-type HAP1 cell lysate at 40 µg
      Lane 2 : LMNA knockout HAP1 cell lysate at 40 µg
      Lane 3 : HeLa cell lysate at 20 µg
      Lane 4 : HepG2 cell lysate at 20 µg

      Performed under reducing conditions.

      Predicted band size: 74 kDa
      Observed band size: 70-75 kDa
      why is the actual band size different from the predicted?


      Exposure time: 150 seconds


      ab196636 was shown to react with Anti-Lamin A + C antibody [JOL2] (HRP) in wild-type HAP1 cells in Western blot. Loss of signal was observed when LMNA knockout sample was used. Membranes were blocked in 3% milk in TBS-T (0.1% Tween®) before incubation with ab196636 overnight at 4°C at a 1 in 200 dilution and ab184095 (Mouse Anti-GAPDH antibody [mAbcam 9484] - Alexa Fluor® 680) at a 1 in 1000 dilution. Blots were developed with Optiblot ECL reagent (ab133456) and imaged.

    • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636)
      Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - HRP Anti-Lamin A + Lamin C antibody [JOL2] (ab196636)

      Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human colon tissue sections labelling Lamin A + C with ab196636.

    Protocols

    • Western blot protocols
    • Immunohistochemistry protocols

    Click here to view the general protocols

    Datasheets and documents

    • Datasheet
    • SDS
  • References (11)

    Publishing research using ab196636? Please let us know so that we can cite the reference in this datasheet.

    ab196636 has been referenced in 11 publications.

    • Sánchez-Osuna M  et al. Caspase-activated DNase is necessary and sufficient for oligonucleosomal DNA breakdown, but not for chromatin disassembly during caspase-dependent apoptosis of LN-18 glioblastoma cells. J Biol Chem 289:18752-69 (2014). Human . PubMed: 24838313
    • Ferreboeuf M  et al. Nuclear protein spreading: implication for pathophysiology of neuromuscular diseases. Hum Mol Genet N/A:N/A (2014). PubMed: 24659496
    • Zhang Y  et al. Human skeletal muscle xenograft as a new preclinical model for muscle disorders. Hum Mol Genet N/A:N/A (2014). Human . PubMed: 24452336
    • Iglesias-Guimarais V  et al. Apoptotic DNA Degradation into Oligonucleosomal Fragments, but Not Apoptotic Nuclear Morphology, Relies on a Cytosolic Pool of DFF40/CAD Endonuclease. J Biol Chem 287:7766-79 (2012). WB ; Human . PubMed: 22253444
    • Mamchaoui K  et al. Immortalized pathological human myoblasts: towards a universal tool for the study of neuromuscular disorders. Skelet Muscle 1:34 (2011). ICC/IF ; Human . PubMed: 22040608
    View all Publications for this product

    Customer reviews and Q&As

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    Question

    ご担当者様


     


    いつもお世話になっております。


    片山化学の土屋と申します。


     


    4月23日頃購入いたしました


    ab196636 Anti-Lamin A + C 抗体 [JOL2] (HRP)  3点


    ユーザー:大阪大学 医学部 未来細胞医療学


    にて、クレームがありました。


    【内容】-20℃保存を推奨されていたのでそのように保存したところ、染色されませんでした。


    陽性コントロールの標本でのラミンの染色結果をお送りします (賦活化条件はすべて同じです。)。


    最初に染色したときにはラミンは陽性に染色されていますが、次に筋肉組織のシワ改善方法を探るために賦活化条件を変えて染色したときに、ラミンは染色されませんでした (染色2回目)。残りの最後の一本の抗体を用いたときにも染色されませんでした (染色3回目)。写真を添付いたしますのでご確認をお願いします。


     


    以上です。


    急ぎご対応いただけますと幸いです。


    ご連絡は


    090-6739-8429 までお願いいたします。


     


    どうぞよろしくお願いいたします。


     


    **************************************


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    土屋 佑介


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    Answer

    いつも大変お世話になっております。


    この度はご購入いただいた製品ab196636につきまして、ユーザー様の期待通りの結果が得られず、申し訳ございませんでした。


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