281M-8

MART-1 (Melan A) (A103) Mouse Monoclonal Antibody

Name: MART-1 (Melan A) (A103) Mouse Monoclonal Antibody
Brand: SIGMA

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NACRES:

NA.41

UNSPSC Code:

12352203

Conjugate:

unconjugated

Clone:

A103, monoclonal

Application:

IHC (p)

Citations:

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Pozwól nam pomóc

biological source

mouse

conjugate

unconjugated

antibody form

culture supernatant

antibody product type

primary antibodies

clone

A103, monoclonal

description

For In Vitro Diagnostic Use in Select Regions (See Chart)

form

buffered aqueous solution

species reactivity

human

packaging

vial of 0.1 mL concentrate (281M-84), vial of 0.5 mL concentrate (281M-85), bottle of 1.0 mL predilute (281M-87), vial of 1.0 mL concentrate (281M-86), bottle of 7.0 mL predilute (281M-88)

manufacturer/tradename

Cell Marque^®

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:100-1:500

isotype

IgG1

control

melanoma

shipped in

wet ice

storage temp.

2-8°C

visualization

cytoplasmic

General description

MART-1 (also known as melan A) is a melanoma antigen recognized by T cells.1-2 MART-1 is a transmembrane protein present in melanocytes of normal skin, nevi, and most melanomas. MART-1 is a useful marker for identifying melanomas.

Physical form

Solution in Tris Buffer, pH 7.3-7.7, with 1% BSA and <0.1% Sodium Azide

Preparation Note

Download the IFU specific to your product lot and formatNote: This requires a keycode which can be found on your packaging or product label.

Analysis Note

IVD

RUO

Other Notes

For Technical Service please contact: 800-665-7284 or email: [email protected]

MART-1 Positive Control Slides, Product No. 281S, are available for immunohistochemistry (formalin-fixed, paraffin-embedded sections).

Legal Information

Cell Marque is a registered trademark of Merck KGaA, Darmstadt, Germany

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Odwiedź Bibliotekę dokumentów

Cloning of the gene coding for a shared human melanoma antigen recognized by autologous T cells infiltrating into tumor.

Y Kawakami et al.

Proceedings of the National Academy of Sciences of the United States of America, 91(9), 3515-3519 (1994-04-26)

By cDNA expression cloning we have isolated a gene encoding a shared human melanoma antigen recognized by HLA-A2 restricted autologous and allogenic tumor-infiltrating lymphocytes (TILs) from patients with metastatic melanoma. By using both transient and stable expression systems, transfection of

Expression of Melan-A and Ki-67 in desmoplastic melanoma and desmoplastic nevi.

Cynthia Kucher et al.

The American Journal of dermatopathology, 26(6), 452-457 (2004-12-25)

Desmoplastic melanoma (DMM) is an uncommon melanoma variant with a distinct morphology, including a prominent spindle cell component with fibrosis, as well as a distinct immunohistochemical profile. Histologically, the spindle cell component of DMM can be confused with sclerotic/desmoplastic nevi

A new gene coding for a differentiation antigen recognized by autologous cytolytic T lymphocytes on HLA-A2 melanomas.

P G Coulie et al.

The Journal of experimental medicine, 180(1), 35-42 (1994-07-01)

It has been reported previously that antitumor cytolytic T lymphocyte (CTL) clones can be isolated from blood lymphocytes of HLA-A2 melanoma patients, after stimulation in vitro with autologous tumor cells, and that some of these CTL clones lyse most HLA-A2

Evaluation of the role of routine melan-A immunohistochemistry for exclusion of microinvasion in 120 cases of lentigo maligna.

Ravi Suchak et al.

The American Journal of dermatopathology, 36(5), 387-391 (2014-01-08)

To assess the usefulness of routine melan-A immunohistochemistry (IHC) for exclusion of microinvasion in lentigo maligna (LM). One hundred and twenty cases of LM from our archives were reviewed by 2 authors with S100 protein and melan-A IHC using a

Differential expression of MART-1 in primary and metastatic melanoma lesions.

T Kageshita et al.

Journal of immunotherapy (Hagerstown, Md. : 1997), 20(6), 460-465 (1997-12-31)

Twenty-eight primary and 29 metastatic melanoma lesions and 18 pigmented nevi lesions were analyzed by using the immunoperoxidase reaction with anti-MART-1 and anti-gp100 monoclonal antibodies (mAbs). The MART-1 was expressed in 28, 29, and 18, and gp100 was expressed in

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