HDTenEightyP/NetNews huggingface dataset:
From: noel@chpc.utexas.edu ((user name unknown))
Subject: VisiCoor -- visualization of proteins
Keywords: visicoor, visualization of proteins 
Organization: The University of Texas System - CHPC
Distribution: bionet
Date: Tue, 7 Apr 92 15:24:15 GMT


Does anyone know how I can get VisiCoor which 
is a program for protein visualization?

This program has described in:

D.A. Kuznetsov and H.A. Lim
"VisiCoor -- A simple program for visualization of proteins"
Journal of Molecular Graphics, 1991(?)

Does anyone have the email address of the authors?

Also does anyone have the email address of E. Hamori
who seems to have done a lot of work on H-trees and H-curves 
for characterization of protein and DNA sequences.

-- 
Noel Menezes                            Internet: noel@hermes.chpc.utexas.edu
Research Assistant                      BITNET:   noel@uthermes
Center for High Performance Computing   Phone:    (512) 471-2447
Balcones Resarch Center & UT-Austin     Fax:      (512) 471-2445
From: C749SCB@SEMOVM.SEMO.EDU (Walt Lilly)
Newsgroups: bionet.molbio.proteins
Subject: protease mutants in fungi
Date: 9 Apr 92 14:06:06 GMT
Distribution: bionet

Apparently, a message I sent several days ago was aborted so here goes a
second try.  We are attempting to isolate mutants for specific proteases
from a wood-decaying fungus.  Does anyone have suggestions for a
selection scheme that might work?  We know that the proposition will be
complicated by the fact that several different proteases are produced
and secreted.  Both endo and exo proteases are produced by the organism
and some of them are up-regulated during N deprivation.

Is anyone aware of commercially-available peptide substrates conjugated
to a toxin?  I am thinking of something that might release CN, for
example, upon hydrolysis.  Thanks.

************************************************************************
*  WALT LILLY                     *                                    *
*  DEPARTMENT OF BIOLOGY          *  INTERNET: C749SCB@SEMOVM.SEMO.EDU *
*  SOUTHEAST MISSOURI STATE UNIV. *  BITNET: C749SCB@SEMOVM            *
*  CAPE GIRARDEAU, MO 63701       *                                    *
************************************************************************
From: v098p82f@ubvmsb.cc.buffalo.edu (NEUTRINO)
Newsgroups: bionet.molbio.proteins
Subject: xtals of p1 nuclease
Date: 9 Apr 92 14:30:00 GMT
Organization: University at Buffalo
News-Software: VAX/VMS VNEWS 1.41


hello

  I need some advice...I've been trying to crystallize nuclease P1 from
pennecilium citrinum for some time now...with poor results.  The structure
was done{beautiful work might I add} by ARmin LAHM at EMBL.  I've followed
his recipies to the letter but have had no good results......any advice
you could offer would help.I'm curently using a hganging drop
and a sitting drop setup  30% saturated amm.sulfate, 5mM ZnCl against
65% saturated amm. sulfate.

Also..where can i get the primary sequence for phoshpholipase C as well
as the refined structural coordinates? references?


thanks in advance

joe falcone
v098p82f@ubvmsb.cc.buffalo.edu
From: yqdx@vax5.cit.cornell.edu
Newsgroups: bionet.molbio.proteins
Subject: How to compute local protein packing density?
Date: 15 Apr 92 16:05:47 EDT
Distribution: bionet
Organization: Cornell University


  I have a reference by Richards (1974, JMB 82: 1-14) explaining the use of
Voronoi polyhedra to compute local packing density in a protein structure. As
Richards states, there are some problems with the technique.  I am wondering if
anybody knows of any refinements of the technique that take account of
different van der Waals radii, while still prefectly filling space.  Thanks in
advance.
-Chris Bruns
Cornell biochemistry grad student
yqdx@vax5.cit.cornell.edu

Newsgroups: bionet.molbio.proteins
From: laub@castor.fccc.edu (Paul Laub)
Subject: protein ribbon diagrams
Organization: Fox Chase Cancer Center
Date: Fri, 10 Apr 1992 15:27:24 GMT

Dear Fellow Protein Modellers,
	I am interested in generating a Jane Richardson-style ribbon
diagram of cytochrome C including the heme. In the past, with simple
proteins lacking prosthetic groups, I have found ribbon program by
Priestle and Callahan/Gleason/Lybrand (part of QCPE #594) very satisfactory.
However, this program works only with the alpha carbons of the backbone.
	Does anyone know whether modifications of this (or other programs)
exist to handle the heme? I use an SGI Personal Iris 4D25TG with Irix 3.3.

Sincerely, Paul Laub
	   Fox Chase Cancer Center, Philadelphia
	   (215) 728-2840/-2748
From: mrigank@aiims.ernet.in
Newsgroups: bionet.molbio.proteins
Subject: Send info
Date: 6 Apr 92 19:39:36 GMT
Distribution: bionet

Please send subscription fo rthis service
Dr. Mrigank, BIophysics
From: C749SCB@SEMOVM.SEMO.EDU (Walt Lilly)
Newsgroups: bionet.molbio.proteins
Subject: protease mutants in fungi
Date: 7 Apr 92 22:30:26 GMT
Article-I.D.: SEMOVM.07APR92.17827888.0011.MUSIC
Distribution: bionet

EDIT INPUT
EDIT
OFF
END
From: martel@marvin.mr.sintef.no (Paulo Martel)
Newsgroups: bionet.molbio.proteins
Subject: Re: protein ribbon diagrams
Date: 14 Apr 92 14:53:40 GMT
Organization: University of Trondheim, Norway

laub@castor.fccc.edu (Paul Laub) writes:

>Dear Fellow Protein Modellers,
>	I am interested in generating a Jane Richardson-style ribbon
>diagram of cytochrome C including the heme. In the past, with simple
>proteins lacking prosthetic groups, I have found ribbon program by
>Priestle and Callahan/Gleason/Lybrand (part of QCPE #594) very satisfactory.
>However, this program works only with the alpha carbons of the backbone.
>	Does anyone know whether modifications of this (or other programs)
>exist to handle the heme? I use an SGI Personal Iris 4D25TG with Irix 3.3.

Try MOLSCRIPT from Per Kraulis, J.appl.Crystallogr. 24:946-950(1991).
I believe the program is available from the author upon request.

Paulo

--
Paulo Martel             |  e-mail: martel@marvin.mr.sintef.no |               
MR-Center                |  phone: +47-7-997700                |               
SINTEF		         |  FAX:   +47-7-997708                |               
N-7034 Trondheim, NORWAY |                                     |
From: C749SCB@SEMOVM.SEMO.EDU (Walt Lilly)
Newsgroups: bionet.molbio.proteins
Subject: protease mutants in fungi
Date: 7 Apr 92 22:30:16 GMT
Article-I.D.: SEMOVM.07APR92.17824912.0011.MUSIC
Distribution: bionet

EDIT INPUT
EDIT
OFF
END
From: sundvall@perrier.embnet.se (Mats Sundvall)
Newsgroups: bionet.molbio.gene-linkage
Subject: Re: LINKAGE speed up
Date: 15 Apr 92 08:54:16 GMT
Reply-To: sundvall@perrier.embnet.se
Organization: EMBNet Project Sweden


In article 11258@gazette.bcm.tmc.edu, bwc@raven.mbir.bcm.tmc.edu (Robert Cottingham) writes:
>
>
>First I want to thank all of the people who responded to my request
>last month for information regarding LINKAGE in C.  The upshot is that
>using p2c to translate the code seems to be totally successful in our
>experience so far.  Several of the respondents also related their
>surprize at how well p2c worked.  To date I am unaware of any human
>modification necessary to use the C code out of p2c.  We are working
>in a Sun environment.

We came to the same conclusion a year ago. We were as surprised as you!

[Suggested change to the code deleted]

>Dont take my word for the accuracy of this code as I havent tried it
>in Pascal yet, but it works in C.  This one change makes about a
>factor of 2 speed improvement.  Again, keep in mind that this code
>change needs to be made in all of the various -seg--- routines that
>contain the *** line of code, in order to see the speed up in all
>situations.

Here you spot a problem with the way the code is organized today without
suggesting the obvious solution. At least 90% of the code in the different
programs (MLINK, ILINK, LINKMAO...) are exactly the same, or with very little
differences. We did run a series of diffs and 3diff on the code and was
able to merge most of the code. Actually you can see the the same change
has been done at several places in the Pascal code, with subtle differences
between the programs. This code is a nightmare to maintain. It should be
easy to merge all these routines into a library of callable routines
without to much work. We did it but did not finish it because we choked
on some routines were we could not understand the code ;-{

To make such a library would make it possible to then go in and optimize
routines and just relink the programs. Of course you do not want to
do it all over again when the next release of Pascal LINKAGE comes out.
That was the other reason we did not finish the work.

Regards,

Mats Sundvall
Dept of Medical Genetics,
Uppsala University
Sweden



>
>If you are going to try p2c and/or the above code changes, I recommend
>that you rerun any final results with the original programs before
>publishing them.
>
>Regards,
>Bob
>
>	------------------------------------------------------------
>	Bob Cottingham          	Phone:  713/798-4275
>	Cell Biology, M301          	Fax:        798-5386
>	Baylor College of Medicine	Email: bwc@bcm.tmc.edu
>	Houston, TX   77030
>	------------------------------------------------------------
Newsgroups: bionet.molbio.ageing
From: jmasters@magnus.acs.ohio-state.edu (Jeffrey N Masters)
Subject: Re: ageing as an evolutionary force
Organization: The Ohio State University
Distribution: bionet
Date: Thu, 16 Apr 1992 19:24:30 GMT

Talk has centered around an imortality gene giving a reproductive
advantage to that species. How true would this be? Most female
mammals undergo reproductive senesence long before mortality. Thus
many more processes would have to be modified to maintain
reproductive senencence in immortal creatures.

In terms of long lived, slow critters. Why wouldn't natural selection
work on animals with an immortality gene in addition to those
critters without such a gene?

Jeff Masters
Newsgroups: bionet.molbio.ageing
From: donnel@helix.nih.gov (Donald A. Lehn)
Subject: Re: Ageing as an evolutionary force.
Organization: National Institutes of Health, Bethesda
Distribution: bionet
Date: Wed, 15 Apr 1992 20:46:21 GMT

I've been reading the posts on this subject and would like to pose a
question?

Why does ageing necessarily have anything to do with DNA damage?  Not
all of the information content of DNA is contained in the nucleotide
sequence.  It may also be likely that ageing is due to a disruption of
chromatin structure.  Perhaps even with something like when a gene
is replicated in mitosis.  I think ageing is a far more complex than
can be described in narrow terms.


--
Donald A. Lehn, Ph.D.                      Phone: (301) 496-2885
Bldg.37 Rm 3D20                            FAX:   (301) 496-8419
National Cancer Institute / NIH            Email: donnel@helix.nih.gov
Bethesda MD 20892
Newsgroups: bionet.molbio.ageing
From: eric@bcserv.wustl.edu (Eric R. Hugo)
Subject: Re: The foutain of youth?
Organization: Washington University in Saint Louis, Missouri USA
Distribution: bionet
Date: Wed, 15 Apr 1992 03:56:02 GMT

I'd like to point out some possible wrong assumptions with the previous
post on this subject.

Firstly, at least in reproduction, the complex patterns of methylation
that have been seen in somatic cells (but not fully understood) are not
necessarily maintained in germ cells.  In most (if not all systems)
germ cells are partitioned away from somatic cells very early in the
developmental process, and thus remain totipotent.  There are a few
examples of nuclear transplantation experiments where somatic
nuclei have been transplanted into enucleated/fertilized ova.  To the
best of my knowledge, the most developed organism that this has been
sucessful with has been amphibians and that was using nuclei from
tadpole somatic cells (ie. not fully developed).  There have been some
claims of experiments using mammalian nuclear transplants but as far
as I know these are very controversial.  This should point out that
the fertilization/early embryonic development does NOT 'renew' the
potency of the hereditary material.
     As to error correction during fertilization, I do not believe this
to be a factual statement.  This is not to say that there isn't DNA
repair occurring, just that there is no comparison between parental strands
To the best of my knowledge, there is no
mechanism for comparing DNA strands between parents.  If you think about
this, first how would the replication repair machinery Know which was
the correct strand, and secondly there is no reason to believe that the
genetic material from one parent would be identical to the other.
As far as I know the only time Holliday structures and the like are formed
between HOMOLOGs as opposed to chomatids is during meiotic (prophase I)
division in sex cell development.
     All of the preceding is not to say that someday it MIGHT be possible
to grow a new body or rejuvenate an old one, but given today's level
of expertese I think we have a ways to go.
-- 
  Eric R. Hugo, Postdoctoral Research Associate |eric@bcserv.wustl.edu
  Dept. of Biochemistry and Molecular Biophysics|                
  Washington University School of Medicine      |               
  Box 8231, St. Louis, MO 63110_________________| (314) 362-3342
From: ST801833@BROWNVM.BROWN.EDU (Rob Krochmal)
Newsgroups: bionet.molbio.ageing
Subject: Re: ageing as an evolutionary force
Date: 16 Apr 92 01:07:10 GMT
Article-I.D.: genbank.9204160133.AA04811
Distribution: bionet

>>    There is a fatal flaw in this particular argument.  Natural selection
>> works on individuals.  If an individual were to develop the aging process
>> as a way to get rid of itself (dead weight), then this individual would have
>> less an advantage at passing its genes to the next generation than one
>> who could stay alive and produce more offspring.
>
>I don't see the flaw.  Organisms don't get rid of themselves - orther oganisms
>do it for them (ie gazelles don't eat gazelles, tigers do).  If a species or
>sub-group within a species developed an immortality gene then the genetic
>variation within the group would quickly diminish     ... and...
>the new high-performance tigers would quickly eat all of the slow but
>immortal gazelles.
>
>Perhaps if such an immortality gene ever existed, it became extinct several
>billion years ago.  In geologic time, the appearance of an immortality gene
> would
>almost certainly result in the extinction of a species unless that species
>enemies before it aquired the immortality gene.
>
You're right, but the scenerio is still worth thinking about.  Gazelles don't
EAT other gazelles, but they do COMPETE with other gazelles for food, mates,
etc.  Therefore, if one were to aquire the immortality gene at some time in
the past, it would enjoy a reproductive advantage (for quite some time),
because it could "endlessly" keep reproducing and passing the immortality
gene to its offspring.  Then gazelles with this gene would replace just about
all others without it.  Finally, due to a combination of population growth,
and a diminishing amount of variability, these gazelles would be at a disad-
vantage, and the ones without it could once again flourish.
From: ODONNELL@ARCB.AFRC.AC.UK (Cary O'Donnell)
Newsgroups: bionet.molbio.ageing
Subject: RE: Ageing and reproduction
Date: 3 Apr 92 10:34:00 GMT
Article-I.D.: genbank.9204071241.AA28148
Distribution: bionet

My first mail:

> > Gamete producing cells appear to constitute the only 'immortal' cell line.

... stuff deleted

> >Ageing is probably a side effect of differentiation,
> > most cells losing the immortality function found in the (undifferentiated?)
> > gamete-producing cells.

David Cooke replied:

> 	I don't see why the time of differentiation should make a
> difference in terms of DNA damage.  DNA gets damaged through chemical
> or radiation-induced mutations and through errors in replication.  Germ
> cells are likely to receive as much damage from chemical and radiation
> agents as any other cells in the body--that's basically a matter of

 If you damage a gamete too much it will probably be immediately lethal.
 Therefore no embryo. It is suspected that some 30% or more of all
 human conceptions don't get to the embryonic stage. Yes - gametes are
 liable to these environmental shocks. But the cell line doesn't "age".

> resemble it).  I think there's much more evidence to suggest that we
> get old because we are programmed to get old, not because we have to
> get old.

Yes - my point exactly. Differentiation of cells impiles the cell specialising
in a set of functions, at the expense of all the others. In gene-expression
terms this means inducing one set of genes and keeping all the others turned
off. Methylation of DNA occurs during embryogenesis. It is believed this is
part of the mechaism that shuts off gene expression permanently in some parts
of the genome.

I admit the gamete cell line is a special case. Maybe some differentiated
cell lines are just as 'immortal' and they get let down by the rest of the
body dying on them :-)


Cary

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-----------------------------------------------------------------------------
Newsgroups: bionet.molbio.ageing
From: house@athena.mit.edu (Daniel J Housman)
Subject: Ageing as an evolutionary force
Organization: Massachusetts Institute of Technology
Distribution: bionet
Date: Tue, 14 Apr 1992 16:20:49 GMT

--------------


	The question has been raised that if the cells in the germ lines
of living organisms have the capability to keep DNA nearly perfectly
intact under attack from free radicals why then is it that the cells
all over the organism are not able to protect themselves in this same manner.
This is a topic that I don't claim to have any expertice but I am 
willing to offer some speculation upon the matter. 
	Ageing like flowering in angiosperms could be an evolutionary 
advantage that promotes recombination and thereby promotes diversity 
that allows survivability. People generally think that aging is a
process which is necessary and a process that must occur merely because
the world is too harsh for an organism to survive in it intact defeating 
entropy for a prolonged period of time. This is not completely 
sensible. It is possible to produce cell lines of cancer cells that 
are essentially immortal. The machinery for immortality exists and were it
to be evolutionarily advantageous to not age and live forever then the
world would have evolved with organisms that were immortal. 
	The reasons why the aging process is useful evolutionarily are as
follows. If there were not a younger generation and an older generation there
would be intermating between generations causing a lack of recombination
that would normally be caused by the constant reshuffling of genes from one
generation to the next. The reproductively active cycles of the organism 
may at one point become inactive to prevent the overexertion of any one
single genotyope during non-selective conditions. Menopause is an example
of this sort. The overexertion would cause a lack of variability in the 
population as a whole and under selective conditions populations with large
amounts of variation would survive. There is no great advantage to staying 
alive longer since major injuries occur making the organism less fit such
as the loss of limbs. The degeneration of the body could be a way to get
rid of the dead weight in the population that would be competing for energy 
 sources so the partially destroyed organisms would be eliminated through an
aging process. Remember that evolution did not occur during the cushy 
non-selective times like today and the immortal organisms would simply 
proliferate without the ability to disappear giving them the problem of
having a lack of adaptability. 
	What this would mean is that there are some inherent causes of aging 
that ought to be conserved throughout the cells of all organisms and the 
DNA must somehow code for this process. This process is probably one of
the fundamental processes of biology and deserves some attention to its
biochemistry. The research that would need to be done would be what factors
be it flaws in the DNA or cellular clocks are causing aging and how can they
be manipulated.

Dan Housman 
95 MIT
From: french@RUST.ZSO.DEC.COM
Newsgroups: bionet.molbio.ageing
Subject: Foutain of youth
Date: 16 Apr 92 01:07:22 GMT
Distribution: bionet


> Fatal flaw:  Most metazoans (multi-cellular animals) do not methylate
> their DNA to a detectable extent.  A particular example is Drosophila,
> which clearly ages.  Methylation in metazoans largely appears to be
> a mammalian anomaly.

Not a fatal flaw:  To obtain the foutain of youth, you must be able to freeze 
the current state information in each cell of your body (or at least be able to
restore it to a previously saved state from time to time).  Part of the state
information that one would need to save is what set of genes that are currently
being expressed.  In mammals,  methlyation/demethlyation of DNA plays an 
important role in switching gene expression on and off.
From: ST801833@BROWNVM.BROWN.EDU (Rob Krochmal)
Newsgroups: bionet.molbio.ageing
Subject: Re: Ageing as an evolutionary force
Date: 15 Apr 92 00:20:57 GMT
Distribution: bionet

(Reply to Dan's posting)
The main point of your suppositions may well be true, but there are some
errors in your thinking:

>Ageing as an evolutionary force
>                           People generally think that aging is a
>process which is necessary and a process that must occur merely because
>the world is too harsh for an organism to survive in it intact defeating
>entropy for a prolonged period of time. This is not completely
>sensible. It is possible to produce cell lines of cancer cells that
>are essentially immortal. The machinery for immortality exists and were it
>to be evolutionarily advantageous to not age and live forever then the
>world would have evolved with organisms that were immortal.

       -Yes, but cancer cells themselves are evidence of entropy causing
the normal cells to malfunction.


>        The reasons why the aging process is useful evolutionarily are as
>follows. If there were not a younger generation and an older generation there
>would be intermating between generations causing a lack of recombination
>that would normally be caused by the constant reshuffling of genes from one
>generation to the next. The reproductively active cycles of the organism
>may at one point become inactive to prevent the overexertion of any one
>single genotyope during non-selective conditions. Menopause is an example
>of this sort. The overexertion would cause a lack of variability in the
>population as a whole and under selective conditions populations with large
>amounts of variation would survive. There is no great advantage to staying
>alive longer since major injuries occur making the organism less fit such
>as the loss of limbs. The degeneration of the body could be a way to get
>rid of the dead weight in the population that would be competing for energy
> sources so the partially destroyed organisms would be eliminated through an
>aging process. Remember that evolution did not occur during the cushy
>non-selective times like today and the immortal organisms would simply
>proliferate without the ability to disappear giving them the problem of
>having a lack of adaptability.

   There is a fatal flaw in this particular argument.  Natural selection
works on individuals.  If an individual were to develop the aging process
as a way to get rid of itself (dead weight), then this individual would have
less an advantage at passing its genes to the next generation than one
who could stay alive and produce more offspring.
      In order to use this argument as a way of explaining aging, one would
have to get around this error.