50-155-7366

TSC1 Polyclonal Antibody, Bethyl Laboratories

Manufacturer: Bethyl Laboratories, Inc

Select a Size

Pack Size SKU Availability Price
Each of 1 50-155-7366-Each-of-1 In Stock ₹ 12,384.35

50-155-7366 - Each of 1

₹ 12,384.35

In Stock

Quantity

1

Base Price: ₹ 12,384.35

GST (18%): ₹ 2,229.183

Total Price: ₹ 14,613.533

Antigen

TSC1

Classification

Polyclonal

Formulation

TBS with 0.1% BSA and 0.09% sodium azide

Gene Accession No.

Q92574, Q9EP53

Gene Symbols

TSC1

Immunogen

Between 1100 and C-term

Quantity

20 μL

Primary or Secondary

Primary

Target Species

Human, Mouse

Product Type

Antibody

Isotype

IgG

Applications

Western Blot

Conjugate

Unconjugated

Gene

TSC1

Gene Alias

Hamartin; Tuberous sclerosis 1 protein; TSC1; KIAA0243; TSC

Host Species

Rabbit

Purification Method

Antigen affinity chromatography

Regulatory Status

RUO

Gene ID (Entrez)

64930, 7248

Content And Storage

4° C

Form

Liquid

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Description

  • The recommended shelf life for this product is 1 year from date of receipt
  • Implicated as a tumor suppressor
  • May have a function in vesicular transport
  • Interaction between TSC1 and TSC2 may facilitate vesicular docking.Defects in TSC1 are the cause of tuberous sclerosis complex (TSC)
  • The molecular basis of TSC is a functional impairement of the hamartin-tuberin complex
  • TSC is an autosomal domit multi-system disorder that affects especially the brain, kidneys, heart, and skin
  • TSC is characterized by hamartomas (benign overgrowths predomitly of a cell or tissue type that occurs normally in the organ) and hamartias (developmental abnormalities of tissue combination)
  • Clinical symptoms can range from benign hypopigmented macules of the skin to profound mental retardation with intractable seizures to premature death from a variety of disease-associated causes.Defects in TSC1 may be a cause of focal cortical dysplasia of Taylor balloon cell type (FCDBC)
  • FCDBC is a subtype of cortical displasias linked to chronic intractable epilepsy
  • Cortical dysplasias display a broad spectrum of structural changes, which appear to result from changes in proliferation, migration, differentiation, and apoptosis of neuronal precursors and neurons during cortical development.