Anti-Lamin A + C antibody [EPR4100] - Nuclear Envelope Marker (ab108595)

Overview

  • Product nameAnti-Lamin A + C antibody [EPR4100] - Nuclear Envelope Marker
    See all Lamin A + C primary antibodies
  • Description
    Rabbit monoclonal [EPR4100] to Lamin A + C - Nuclear Envelope Marker
  • SpecificityThe antibody recognizes full length Lamin A/C and the cleaved large unit. We have data to indicate that this antibody gives non-specific staining in IHC with mouse tissues. Based on this we believe the antibody is not suitable for use with mouse samples, as there will be non-specific staining.
  • Tested applicationsSuitable for: ICC/IF, WB, IP, IHC-P, Flow Cytmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Synthetic peptide (the amino acid sequence is considered to be commercially sensitive) corresponding to Human Lamin A + C aa 500-600.

  • Positive control
    • WB: HeLa, HepG2, HACAT and SH-SY5Y cell lysates. IHC-P: Human brain, liver, cervix carcinoma, breast carcinoma, urothelial carcinoma and colonic carcinoma tissues. ICC/IF HeLa cells. Flow Cyt: HeLa cells.
  • General notes

    This product is a recombinant rabbit monoclonal antibody.

    We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated ‘PUR’ on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.

    Produced using Abcam’s RabMAb® technology. RabMAb® technology is covered by the following U.S. Patents, No. 5,675,063 and/or 7,429,487.

    A trial size is available to purchase for this antibody.

    Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species. Please contact us for more information.

    Alternative versions available:

    Anti-Lamin A + C antibody (Phycoerythrin) [EPR4100] - Nuclear Envelope Marker (ab210433)

    Anti-Lamin A + C antibody (Alexa Fluor® 488) - Nuclear Envelope Marker [EPR4100] (ab185014)

    Anti-Lamin A + C antibody (Alexa Fluor® 647) - Nuclear Envelope Marker [EPR4100] (ab193903)

    Anti-Lamin A + C antibody (HRP) - Nuclear Envelope Marker
    [EPR4100] (ab193904)

Properties

Applications

Our Abpromise guarantee covers the use of ab108595 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
ICC/IF 1/250 - 1/500.
WB 1/10000 - 1/50000. Predicted molecular weight: 63,74 kDa.
IP 1/30.
IHC-P 1/250 - 1/500. Perform heat mediated antigen retrieval with Tris/EDTA buffer pH 9.0 before commencing with IHC staining protocol.

See protocols (link: http://www.abcam.com/protocols/ihc-antigen-retrieval-protocol).

Flow Cyt 1/100 - 1/150. ab172730-Rabbit monoclonal IgG, is suitable for use as an isotype control with this antibody.

Target

  • FunctionLamins 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 specificityIn 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 diseaseDefects 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 similaritiesBelongs 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 localizationNucleus. 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.
  • Information by UniProt
  • Database links
  • 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/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

Anti-Lamin A + C antibody [EPR4100] - Nuclear Envelope Marker images

  • Anti-Lamin A + C antibody [EPR4100] - Nuclear Envelope Marker (ab108595) at 1/100000 dilution (purified) + HeLa cell lysate at 10 µg

    Secondary
    Peroxidase-conjugated goat anti-rabbit IgG (H+L) at 1/1000 dilution

    Predicted band size : 63,74 kDa
    Observed band size : 63,74 kDa

    Blocking buffer and concentration: 5% NFDM/TBST.

    Diluting buffer and concentration: 5% NFDM /TBST.

  • All lanes : Anti-Lamin A + C antibody [EPR4100] - Nuclear Envelope Marker (ab108595) at 1/100000 dilution (purified)

    Lane 1 : HepG2 cell lysate
    Lane 2 : HACAT cell lysate

    Lysates/proteins at 20 µg per lane.

    Secondary
    Peroxidase-conjugated goat anti-rabbit IgG (H+L) at 1/1000 dilution

    Predicted band size : 63,74 kDa
    Observed band size : 63,74 kDa

    Blocking buffer and concentration: 5% NFDM/TBST.

    Diluting buffer and concentration: 5% NFDM /TBST.

  • All lanes : Anti-Lamin A + C antibody [EPR4100] - Nuclear Envelope Marker (ab108595) at 1/10000 dilution (unpurified)

    Lane 1 : HeLa cell lysates
    Lane 2 : SH-SY5Y cell lysates

    Lysates/proteins at 10 µg per lane.


    Predicted band size : 63,74 kDa
  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human cervix carcinoma tissue labelling Lamin A + C with purified ab108595 at 1/250. Heat mediated antigen retrieval was performed using Tris/EDTA buffer pH 9. A prediluted HRP-polymer conjugated anti-rabbit IgG was used as the secondary antibody. Negative control using PBS instead of primary antibody. Counterstained with Hematoxylin.

  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human brain tissue labelling Lamin A + C with ab108595 at 1/250 dilution.

  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human liver tissue labelling Lamin A + C with ab108595 at 1/250 dilution.

  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human breast carcinoma tissue labelling Lamin A + C with ab108595. Green - Lamin A + C, Red - PI.

  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human cervical carcinoma tissue labelling Lamin A + C with ab108595. Green - Lamin A + C, Red - PI.

  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human urothelial carcinoma tissue labelling Lamin A + C with ab108595. Green - Lamin A + C, Red - PI.

  • Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) analysis of human colonic carcinoma tissue labelling Lamin A + C with ab108595. Green - Lamin A + C, Red - PI.

  • Immunocytochemistry/Immunofluorescence analysis of HeLa cells labelling Lamin A + C (green) with purified ab108595 at 1/500. Cells were fixed with 4% paraformaldehyde and permeabilized with 0.1% Triton X-100. ab150077, an Alexa Fluor® 488-conjugated goat anti-rabbit IgG (1/500) was used as the secondary antibody. DAPI (blue) was used as the nuclear counterstain.

    Control: primary antibody (1/500) and secondary antibody ab150120, an Alexa Fluor® 594-conjugated goat anti-mouse IgG (1/500).

  • Immunocytochemsitry/Immunofluorescence analysis of HeLa cells labelling Lamin A + C with unpurified ab108595 at 1/250 dilution.

  • Flow Cytometry analysis of HeLa cells labelling Lamin A + C with purified ab108595 at 1/110 (red). Cells were fixed with 2% paraformaldehyde. A FITC-conjugated goat anti-rabbit IgG (1/150) was used as the secondary antibody. Black - Isotype control, rabbit monoclonal IgG. Blue - Unlabelled control, cells without incubation with primary and secondary antibodies.

  • Overlay histogram showing HeLa cells stained with unpurified ab108595 (red line). The cells were fixed with 80% methanol (5 min) and then permeabilized with 0.1% PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab108595, 1/1000 dilution) for 30 min at 22°C. The secondary antibody used was Alexa Fluor® 488 goat anti-rabbit IgG (H&L) (ab150077) at 1/2000 dilution for 30 min at 22°C. Isotype control antibody (black line) was rabbit IgG (monoclonal) (0.1μg/1x106 cells) used under the same conditions. Unlabelled sample (blue line) was also used as a control. Acquisition of >5,000 events were collected using a 20mW Argon ion laser (488nm) and 525/30 bandpass filter.

  • ab108595 (purified) at 1/30 immunoprecipitating Lamin A + C in HeLa cell lysate. For western blotting, a peroxidase-conjugated goat anti-rabbit IgG (H+L) was used as the secondary antibody (1/1000).

    Blocking buffer and concentration: 5% NFDM/TBST.

    Diluting buffer and concentration: 5% NFDM /TBST.

References for Anti-Lamin A + C antibody [EPR4100] - Nuclear Envelope Marker (ab108595)

This product has been referenced in:
  • Kang H  et al. Small molecule-driven direct conversion of human pluripotent stem cells into functional osteoblasts. Sci Adv 2:e1600691 (2016). Read more (PubMed: 27602403) »
  • Meyer GA  et al. Epimuscular Fat in the Human Rotator Cuff Is a Novel Beige Depot. Stem Cells Transl Med 4:764-74 (2015). Histology ; Human . Read more (PubMed: 25999520) »

See all 8 Publications for this product

Product Wall

Abcam guarantees this product to work in the species/application used in this Abreview.
Application Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)
Sample Human Tissue sections (Tonsils)
Antigen retrieval step Heat mediated - Buffer/Enzyme Used: Tris-EDTA pH9
Permeabilization No
Specification Tonsils
Blocking step BSA as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 2% · Temperature: 25°C
Fixative Paraformaldehyde
Username

Abcam user community

Verified customer

Submitted May 16 2016

Application Immunohistochemistry (Frozen sections)
Blocking step Serum as blocking agent for 30 minute(s) · Concentration: 10% · Temperature: RT°C
Sample Human Tissue sections (muscle)
Specification muscle
Permeabilization Yes - Triton X100
Fixative no
Username

Abcam user community

Verified customer

Submitted Jan 26 2015

Application Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)
Blocking step BSA as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 1% · Temperature: 25°C
Antigen retrieval step Heat mediated - Buffer/Enzyme Used: ph6 Pressure cooker
Sample Human Tissue sections (human tumour in mouse lung)
Specification human tumour in mouse lung
Permeabilization No
Fixative Formaldehyde
Username

Dr. VIctoria Thompson

Verified customer

Submitted Jun 04 2014

Thank you for yoru recent enquiry. I am sorry it has taken some time to confirm this ifnormatino for you.

In answer to your questions:

1. I am sorry we cannot confirm for sure if ab108595 Lamin Aantibody would be a good antibody f...

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