• Product name

    Anti-Lamin A + Lamin C antibody [131C3]
    See all Lamin A + Lamin C primary antibodies
  • Description

    Mouse monoclonal [131C3] to Lamin A + Lamin C
  • Host species

  • Specificity

    ab8984 reacts with lamins A and C. Lamins do not appear to be universally distributed among different cell and tissue types. ab8984 has been shown to react with HT1080 cells in Western blot. Other cell/tissue types have not been tested. Customer feedback seems to indicate that ab8984 does not detect Lamin A+C in rat brain lysates (please see AbReviews).
  • Tested applications

    Suitable for: IP, Flow Cyt, ICC, IHC-Fr, WB, ICC/IFmore details
  • Species reactivity

    Reacts with: Mouse, Rat, Sheep, Hamster, Cow, Dog, Human
  • Immunogen

    Tissue, cells or virus corresponding to Rat Lamin A + Lamin C. rat liver lamins around aa 319 - 566.

  • Epitope

    Between residues 319-566.
  • Positive control

    • IHC: human colon WB: Human fibroblast, HT1080 cells



Our Abpromise guarantee covers the use of ab8984 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
IP Use at an assay dependent concentration. PubMed: 16126733
Flow Cyt 1/100 - 1/200.

ab170190 - Mouse monoclonal IgG1, is suitable for use as an isotype control with this antibody.

ICC Use at an assay dependent concentration. Fix cells in precold (- 20°C) 1:1 methanol/acetone for 20 minutes at - 20°C.
IHC-Fr Use at an assay dependent concentration. Recommended range is 1/100 - 1/200 for Immunohistochemistry with avidin-biotinylated horseradish peroxidase complex (ABC) as detection reagent.
WB 1/100 - 1/1000. Predicted molecular weight: 70 kDa. Use nuclear extracts, incubate primary antibody overnight. Predicted molecular weight: 65-70 kDa depending on the species and preparation.
ICC/IF Use at an assay dependent concentration. Used at an a dilution of 1/200 (for 16 hrs incubation) on HeLa cells (see Abreview for further information).


  • 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

    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.
  • 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 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


  • IHC-Fr of human colon showing nuclear lamina staining in epithelial and connective tissue cells.

  • ab8984 at a 1/200 dilution staining Asynchronous and paraformaldehyde-fixed (4%) HeLa cells by immunocytochemistry. The antibody was incubated with the cells overnight and then detected using a Cy3 conjugated Goat Anti-Mouse IgG (H+L) antibody (ab97035). The image shows faint, but distinct, nuclear membrane staining.

    This image is courtesy of an Abreview by Kirk McManus submitted on 27 February 2006.

    See Abreview

  • Anti-Lamin A + Lamin C antibody [131C3] (ab8984) at 1/100 dilution + human fibroblast at 15 µl

    Developed using the ECL technique.

    Performed under reducing conditions.

    Predicted band size: 70 kDa

    ab8984 was used at a 1:100 dilution against human fibroblast lysate. Lamin A and C are detected. Lysates were prepared in RIPA buffer on ice for 30 min. They were sonicated 4 times for 5 sec prior to mixing with loading buffer.
  • Overlay histogram showing HeLA cells stained with ab8984 (red line). The cells were fixed with 100% 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 (ab7481)  / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab8984, 1µg/1x106 cells) for 30 min at 22°C. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (ab96879) at 1/500 dilution for 30 min at 22°C. Isotype control antibody (black line) was Mouse IgG1 [ICIGG1] (ab91353, 2µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed.

  • ab8984 staining dog skeletal muscle tissue cells by ICC/IF.  Cells were fixed in methanol and incubated with ab8984, diluted 1/200, for 12 hours at 4°C.  A FITC conjugated goat anti-mouse antibody (ab6785), diluted 1/200, was used as the secondary antibody.


    See Abreview

  • A. HT1080 cells + siRNA control sequence

    B. HT1080 cells + siRNA Lamin

    A. HT1080 cells + siRNA control sequence

    B. HT1080 cells + siRNA Lamin

  • All lanes : Anti-Lamin A + Lamin C antibody [131C3] (ab8984) at 1/1000 dilution

    Lane 1 : 10ug HeLa whole cell lysate
    Lane 2 : 50ug HeLa whole cell lysate
    Lane 3 : 100ug HeLa whole cell lysate

    All lanes : HRP conjugated goat anti-mouse antibody

    Developed using the ECL technique.

    Predicted band size: 70 kDa
    Observed band size: 70 kDa

    Exposure time: 30 seconds

    See Abreview


This product has been referenced in:

  • Méndez-López I  et al. Hippocampal LMNA Gene Expression is Increased in Late-Stage Alzheimer's Disease. Int J Mol Sci 20:N/A (2019). Read more (PubMed: 30781626) »
  • Grigoryan A  et al. LaminA/C regulates epigenetic and chromatin architecture changes upon aging of hematopoietic stem cells. Genome Biol 19:189 (2018). Read more (PubMed: 30404662) »
See all 38 Publications for this product

Customer reviews and Q&As

1-10 of 27 Abreviews or Q&A

Western blot
Pig Cell lysate - nuclear (fibroblasts)
Gel Running Conditions
Reduced Denaturing (10% Tris-glycine)
Loading amount
40 µg
Blocking step
Milk as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 5% · Temperature: 21°C

Ms. Maeve Ballantyne

Verified customer

Submitted Dec 22 2015

Western blot
Human Cell lysate - whole cell (HeLa, RPE-1)
Loading amount
36 µg
HeLa, RPE-1
Gel Running Conditions
Reduced Denaturing (4-12%)
Blocking step
Milk as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 10% · Temperature: 23°C

Abcam user community

Verified customer

Submitted May 01 2013

Western blot
Rat Tissue lysate - nuclear (liver)
Loading amount
30 µg
Gel Running Conditions
Reduced Denaturing (10%)
Blocking step
Milk as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 1% · Temperature: 25°C

Abcam user community

Verified customer

Submitted Apr 16 2013


Thank you for your email. I am sorry to hear that you have been experiencing problems with this antibody.

I have read the details you have kindly provided and have following further suggestions;

The antibody has been tested in ICC/IF and WB and is fully guaranteed. The protocol looks fine to me so I am sorry we are unable to find the cause of the problem. As the antibody is working in ICC/IF so the quality of antibody can also not be questioned.

The only way to check, whether the problem is due to antibody or lysates I would suggest testing whole cell lysates and then observing the results. If the antibody fails we will be happy replacing the ab with different lot. Please do try different dilutions as well e.g. 1/100, 1/200 and 1/500

Thank you very much for your cooperation. I will look forward to hearing from you soon.

Read More


Thank you for contacting us.

I can confirm that any anti mouse antibody that detects the complete IgG isotype or the IgG1 isotype should detect the Anti-Lamin A + C antibody [131C3] - Nuclear Envelope Marker (ab8984).

I reviewed the provided product datasheet and this rabbit anti mouse antibody would fall into this category and should for this reason detect the ab8984.

Could you confirm that the datasheet shows the same antibody the customer refers to? Because the customer seems to use a GOAT anti mouse HRP instead of a rabbit anti mouse HRP.

I hope this information is helpful to you. Please do not hesitate to contact us if you need any more advice or information.

Read More


Thank you for confirming these details and for your cooperation. The details provided enable us to closely monitor the quality of our products.

I am sorry this product did not perform as stated on the datasheet and for the inconvenience this has caused. As requested, I have issued a free of charge replacement with the order number ***.

To check the status of the order please contact our Customer Service team and reference this number.

Please note that this free of charge replacement vial is also covered by our Abpromise guarantee. Should you still be experiencing difficulties, or if you have any further questions, please do not hesitate to let us know.

I wish you the best of luck with your research.

Read More


Thank you for contacting us. I am sorry that ab8984 is giving poor results in WB.

Have you validated your transfer at the higher molecular weights by Ponceau stain? If the transfer is incomplete, that could account for the lack of the specific band. You could try transferring longer or adding 0.1% SDS to the transfer buffer and lowering the methanol percentage to 10%.

If you are able to detect the specific band with these alterations, you may be able to reduce some of the background bands. The bands around 25 and 50 kDa may be due to the secondary antibody cross-reacting with endogenous IgGs (this can be checked by running a no primary antibody control). If you are getting background due to endogenous IgGs, you could switch to a secondary antibody that is specific for native IgGs, such as our VeriBlot secondary ab131368.

Could you please let me know what dilutions and incubation times you were using for your primary and secondary antibodies? What blocking agent was used and at what percentage?

I hope this helps, if not, I will be happy to offer you a free of charge replacement, credit, or refund. Please let me know your original order number and how you would like to proceed and I will be happy to help you help you further.

Read More
Western blot
Human Cell lysate - whole cell (HCT116, colon cancer)
Loading amount
60 µg
HCT116, colon cancer
24 hrs, different treatment
Gel Running Conditions
Reduced Denaturing (13%)
Blocking step
Milk as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 5% · Temperature: 25°C

Mr. Christian Marx

Verified customer

Submitted Aug 21 2012


Thank you for calling us and for alerting us to the problem you are experiencing with our product. We take product complaints very seriously, and investigate every product that we feel may not be performing correctly.

As we discussed on the phone, Ihave attachedour questionnaire so thatI can gather further information regarding the samples tested and the protocol used. OnceI have receive the completed questionnaire,I will look at the protocol and see if there are any suggestions we can make that may improve the results. This information will also allow us to investigate this case internally and initiate additional testing where necessary. If the product was purchased in the last six months and is being used according to our Abpromise, we would be happy to replace or refund the antibody.

I look forward to receiving your reply.

Read More


Thank you for your enquiry.

Below is a selection of antibodies that are suitable for detecting the plasma membrane and nuclear envelope. They all work in western blot and I would review the datasheets to confirm which species they are tested against.

Plasma membrane
ab4645 Anti-Pma1 antibody [40B7]

ab7671 Anti-alpha 1 Sodium Potassium ATPase antibody [464.6]

ab16505 Anti-pan Cadherin antibody

ab22744 Anti-pan Cadherin antibody [mAbcam22744]

Nuclear envelope
ab8980 Anti-Lamin A antibody [133A2]

ab8984 Anti-Lamin A + C antibody [131C3]

ab16048 Anti-Lamin B1 antibody

I hope this is useful. Just let me know if you have further questions.

Read More

1-10 of 27 Abreviews or Q&A

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