MABE230
Anti-SMN2 Antibody, clone SMN-KH
clone SMN-KH, from mouse
Sinonimo/i:
Survival motor neuron protein, Component of gems 1, Gemin-1
Autenticatiper visualizzare i prezzi riservati alla tua organizzazione & contrattuali
About This Item
Codice UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Prodotti consigliati
Origine biologica
mouse
Livello qualitativo
Forma dell’anticorpo
purified immunoglobulin
Tipo di anticorpo
primary antibodies
Clone
SMN-KH, monoclonal
Reattività contro le specie
human
tecniche
immunohistochemistry: suitable
western blot: suitable
Isotipo
IgG1κ
N° accesso NCBI
N° accesso UniProt
Condizioni di spedizione
wet ice
modifica post-traduzionali bersaglio
unmodified
Informazioni sul gene
human ... SMN2(6607)
Descrizione generale
Survival of Motor Neuron (SMN) is expressed from two linked paralogous genes, SMN1 and SMN2. SMNs are primarily localized in the cytoplasm and nuclear gems of all cells, where they are understood to mediate the assembly of spliceosomal small nuclear ribonucleoprotein particles (snRNPs). They also play a role in the metabolism of snoRNPs and are required for the splicing of pre-mRNA in the nucleus. The progressive loss of functional SMNs in the anterior horn of the spinal cord is a critical cause of Spinal Muscular Atrophy (SMA), an autosomal recessive neuromuscular disease. There are three known types of childhood-onset SMA, in addition to a fourth type that is characterized by adult-onset SMA.
Immunogeno
MBP-tagged recombinant protein corresponding to human SMN2.
Applicazioni
Anti-SMN2 Antibody, clone SMN-KH is a Mouse Monoclonal Antibody for detection of SMN2 also known as Survival motor neuron protein & has been validated in WB & IHC.
Western Blot Analysis: A representative lot from an independent laboratory detected SMN2 in HeLa cell lysate.
Immunohistochemistry Analysis: A respresentative lot from an independent laboratory detected human SMN2 in SMA type III mouse model thoracic spinal cord tissue. (Hua, Y., et al. (2010). Genes Dev. 24(15):1634-1644.)
Immunohistochemistry Analysis: A respresentative lot from an independent laboratory detected human SMN2 in SMA type III mouse model thoracic spinal cord tissue. (Hua, Y., et al. (2010). Genes Dev. 24(15):1634-1644.)
Qualità
Evaluated by Western Blot in HeLa cell lysate.
Western Blot Analysis: 0.5 µg/mL of this antibody detected SMN2 in 10 µg of HeLa cell lysate.
Western Blot Analysis: 0.5 µg/mL of this antibody detected SMN2 in 10 µg of HeLa cell lysate.
Descrizione del bersaglio
~35 kDa observed
Stato fisico
Format: Purified
Altre note
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
Not finding the right product?
Try our Motore di ricerca dei prodotti.
Codice della classe di stoccaggio
12 - Non Combustible Liquids
Classe di pericolosità dell'acqua (WGK)
WGK 1
Punto d’infiammabilità (°F)
Not applicable
Punto d’infiammabilità (°C)
Not applicable
Certificati d'analisi (COA)
Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘Batch’.
Possiedi già questo prodotto?
I documenti relativi ai prodotti acquistati recentemente sono disponibili nell’Archivio dei documenti.
Suzan M Hammond et al.
JCI insight, 7(24) (2022-11-09)
Antisense oligonucleotides (ASOs) have emerged as one of the most innovative new genetic drug modalities. However, their high molecular weight limits their bioavailability for otherwise-treatable neurological disorders. We investigated conjugation of ASOs to an antibody against the murine transferrin receptor
Anton J Blatnik et al.
Human molecular genetics, 29(21), 3477-3492 (2020-10-20)
Spinal muscular atrophy (SMA) is caused by mutation or deletion of survival motor neuron 1 (SMN1) and retention of SMN2 leading to SMN protein deficiency. We developed an immortalized mouse embryonic fibroblast (iMEF) line in which full-length wild-type Smn (flwt-Smn)
Anna J Kordala et al.
EMBO molecular medicine, 15(11), e17683-e17683 (2023-09-19)
Spinal muscular atrophy (SMA) is a leading genetic cause of infant mortality. The advent of approved treatments for this devastating condition has significantly changed SMA patients' life expectancy and quality of life. Nevertheless, these are not without limitations, and research
Matthew D Howell et al.
Molecular therapy : the journal of the American Society of Gene Therapy, 25(6), 1328-1341 (2017-04-17)
Spinal muscular atrophy (SMA), the leading genetic disease of children, is caused by low levels of survival motor neuron (SMN) protein. Here, we employ A15/283, an antisense oligonucleotide targeting a deep intronic sequence/structure, to examine the impact of restoration of
Il team dei nostri ricercatori vanta grande esperienza in tutte le aree della ricerca quali Life Science, scienza dei materiali, sintesi chimica, cromatografia, discipline analitiche, ecc..
Contatta l'Assistenza Tecnica.