MIST1/bHLHa15 Antibody [L9C15] | Primary Antibodies

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IHC1:100

Application
WB, IHC

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
23 kDa

Positive Control	Human pancreas; Mouse pancreas; Mouse small intestine; Mouse spleen
Negative Control	Human colon

Datasheet & SDS

Biological Description

Specificity
MIST1/bHLHa15 Antibody [L9C15] detects endogenous levels of total MIST1/bHLHa15 protein.

Clone
L9C15

Synonym(s)
Class A basic helix-loop-helix protein 15; bHLHa15; Class B basic helix-loop-helix protein 8 (bHLHb8); Muscle, intestine and stomach expression 1 (MIST-1); BHLHA15; BHLHB8; MIST1

Background
Class A basic helix-loop-helix protein 15 (MIST1/BHLHA15) is a highly conserved transcription factor in the bHLH family, distinguished by a central bHLH domain that mediates DNA binding at E-box motifs (CANNTG, especially TA-E-boxes) and dimerization, as well as N- and C-terminal activation domains that recruit p300/CBP coactivators through histone acetylation. With a length of about 227 amino acids, MIST1 acts predominantly as a homodimer and can retain most of its transcriptional activity even when truncated to the bHLH core. MIST1 does not determine cell fate but serves as a master “scaling factor” that orchestrates the specialized architecture of secretory exocrine cells, including pancreatic acinar, salivary gland, and gastric chief cells. It establishes apical-basal polarity, directs the organization and positioning of organelles such as zymogen granules, and regulates the cytoskeleton, all of which are essential for efficient regulated exocytosis. MIST1 controls the trafficking of granules by modulating genes such as RAB26 and RAB3D, thereby ensuring that secretory products are delivered accurately and on demand. During endoplasmic reticulum (ER) stress, MIST1 expression is upregulated by XBP1, enabling cells to scale up protein synthesis and folding capacity via the unfolded protein response (UPR), while also providing negative feedback to prevent chronic stress and apoptosis. Loss of MIST1 results in a dramatic breakdown of the secretory apparatus: granules become disorganized and smaller, apical-basal polarity is lost, organelle positioning is disrupted, and cells become highly susceptible to pancreatic injury, acinar-to-ductal metaplasia (ADM), and neoplastic progression.

Background

Class A basic helix-loop-helix protein 15 (MIST1/BHLHA15) is a highly conserved transcription factor in the bHLH family, distinguished by a central bHLH domain that mediates DNA binding at E-box motifs (CANNTG, especially TA-E-boxes) and dimerization, as well as N- and C-terminal activation domains that recruit p300/CBP coactivators through histone acetylation. With a length of about 227 amino acids, MIST1 acts predominantly as a homodimer and can retain most of its transcriptional activity even when truncated to the bHLH core. MIST1 does not determine cell fate but serves as a master “scaling factor” that orchestrates the specialized architecture of secretory exocrine cells, including pancreatic acinar, salivary gland, and gastric chief cells. It establishes apical-basal polarity, directs the organization and positioning of organelles such as zymogen granules, and regulates the cytoskeleton, all of which are essential for efficient regulated exocytosis. MIST1 controls the trafficking of granules by modulating genes such as RAB26 and RAB3D, thereby ensuring that secretory products are delivered accurately and on demand. During endoplasmic reticulum (ER) stress, MIST1 expression is upregulated by XBP1, enabling cells to scale up protein synthesis and folding capacity via the unfolded protein response (UPR), while also providing negative feedback to prevent chronic stress and apoptosis. Loss of MIST1 results in a dramatic breakdown of the secretory apparatus: granules become disorganized and smaller, apical-basal polarity is lost, organelle positioning is disrupted, and cells become highly susceptible to pancreatic injury, acinar-to-ductal metaplasia (ADM), and neoplastic progression.

References
https://pubmed.ncbi.nlm.nih.gov/28174210/ https://pubmed.ncbi.nlm.nih.gov/17605298/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%