Mouse Lamin B1 Peptide

Cat. No.: CLPP-00150187

Product Size: 1 mg Custom size

Product Overview

Description
CLPP-00150187 is synthetic mouse LMNB1 Peptide
Purity
> 70%
Applications
Blocking
Protein Length
Peptide
Animal Free
No
Nature
Synthetic
Species
Mouse
Form
Lyophilized
Sequence
MATATPVPPRMGSRAGGPTTPLSPTRLSRLQEKEELRELNDRLAVYIDKVRSLETENSALQLQVTEREEVRGRELTGLKALYETELADARRALDDTARERAKLQIELGKCKAEHDQLLLNYAKKESDLNGAQIKLREYEAALNSKDAALATALGDKKSLEGDLEDLKDQIAQLEASLAAAKKQLADETLLKVDLENRCQSLTEDLEFRKSMYEEEINETRRKHETRLVEVDSGRQIEYEYKLAQALHEMREQHDAQVRLYKEELEQTYHAKLENARLSSEMNTSTVNSAREELMESRMRIESLSSQLSNLQKESRACLERIQELEDLLAKEKDNSRRMLTDKEREMAEIRDQMQQQLNDYEQLLDVKLALDMEISAYRKLLEGEEERLKLSPSPSSRVTVSRASSSRSVRTTRGKRKRVDVEESEASSSVSISHSASATGNVCIEEIDVDGKFIRLKNTSEQDQPMGGWEMIRKIGDTSVSYKYTSRYVLKAGQTVTIWAANAGVTASPPTDLIWKNQNSWGTGEDVKVILKNSQGEEVAQRSTVFKTTIPEEEEEEEEAAGVVVEEELFHQQGTPRASNRSCAIM
Sequence Similarities
Belongs to the intermediate filament family.

Target Information

Protein Name
LMNB1
UniProt No.
Alternative Names
ADLD; lamin B1; Lamin-B1; LMN; LMN2; LMNB; Lmnb1; LMNB1_HUMAN; MGC111419; OTTHUMP00000159218
Protein 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.
Involvement in Disease
Defects in LMNB1 are the cause of leukodystrophy demyelinating autosomal dominant adult-onset (ADLD). ADLD is a slowly progressive and fatal demyelinating leukodystrophy, presenting in the fourth or fifth decade of life. Clinically characterized by early autonomic abnormalities, pyramidal and cerebellar dysfunction, and symmetric demyelination of the CNS. It differs from multiple sclerosis and other demyelinating disorders in that neuropathology shows preservation of oligodendroglia in the presence of subtotal demyelination and lack of astrogliosis.

Shipping & Handling

Shipping
Shipped at 4 °C.
Storage
Store at -20 °C or -80 °C.

For Research Use Only. Not For Clinical Use.

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